Tag: AIIMS PG

Renal Trauma

Renal Trauma


RENAL INJURY

  • Renal trauma is due to-

a) Minor injuries- blunt trauma (RTA, falls, assaults & sporting injuries)

b) Major injuries – penetrating trauma (knife or gunshot wounds)

  • Blunt trauma is much more common than penetrating trauma.
  • Renal injuries are classified as follows-

1. Grade I-

  • Contusion or non-enlarging subcapsular perirenal haematoma, and no laceration.

2. Grade II-

  • Superficial laceration

3. Grade III-

  • Laceration >1 cm without extension into the renal pelvis or collecting system (no evidence of urine extravasation).

4. Grade IV-

  • Laceration extends to renal pelvis or urinary exrravasatlon.
  • Vascular: injury to main renal artery or vein with contained haemorrhage.
  • Segmental infarctions without associated lacerations.
  • Expanding subcapsular haematomas compressing the kidney.

5. Grade V-

  • Shattered kidney.
  • Avulsion of renal hilum: devascularisation of a kidney due to hilar injury.
  • Ureteropelvicavulsions.
  • Complete laceration or thrombus of the main renal artery or vein.

 

 

Clinical features-

  • Hematuria is the most important sign of renal injury.
  • Loin bulge due to perinephric haemtoma.
  • Bruising of soft tissue in the loin.
  • Retroperitoneal haematoma –> abdominal distension.
  • systolic blood pressure ≤90 mmHg

Investigations-

  1. Intravenous pyelography (IVP) can shows (An IVP is done urgently to assesss the damage to the kidney and to know the functioning of the other kidney)-
  • Intrarenal extravasation
  • Extrarenal extravasation
  • Function of injured kidney

2. CT scan with contrast is the IOC

3. USG

Treatment-

  • Blunt trauma are treated conservatively
  • Penetrating injuries, small & major lacerations- surgical exploration.

Exam Important

  • Renal injuries are classified as follows-

1. Grade I: contusion or non-enlarging subcapsular perirenal haematoma, and no laceration.

2. Grade II: superficial laceration

3. Grade III: laceration >1 cm without extension into the renal pelvis or collecting system (no evidence of urine extravasation).

4. Grade IV

  • Laceration extends to renal pelvis or urinary exrravasatlon.
  • Vascular: injury to main renal artery or vein with contained haemorrhage.
  • Segmental infarctions without associated lacerations.
  • Expanding subcapsular haematomas compressing the kidney.

5. Grade V:

  • Shattered kidney.
  • Avulsion of renal hilum: devascularisation of a kidnev due to hilar injury.
  • Ureteropelvicavulsions.
  • Complete laceration or thrombus of the main renal artery or vein.

 

 

Clinical features-

  • Hematuria is the most important sign of renal injury.
  • Loin bulge due to perinephric haemtoma.
  • Bruising of soft tissue in the loin.
  • Retroperitoneal haematoma –> abdominal distension.
  • systolic blood pressure ≤90 mmHg

 

Investigations-

  1. Intravenous pyelography (IVP) can shows-
  • Intrarenal extravasation
  • Extrarenal extravasation
  • Function of injured kidney

2. CT scan with contrast is the IOC

3. USG

 

 

Don’t Forget to Solve all the previous Year Question asked on Renal Trauma

Module Below Start Quiz

Renal Trauma

Renal Trauma

Q. 1

Which of the following is true about renal trauma‑

 A Urgent IVP is indicated

 B

Exploration of the kidney to be done in all cases

 C

Lumbar approach to kidney is preferred

 D

Renal artery aneurysm is common

Q. 1

Which of the following is true about renal trauma‑

 A

Urgent IVP is indicated

 B

Exploration of the kidney to be done in all cases

 C

Lumbar approach to kidney is preferred

 D

Renal artery aneurysm is common

Ans. A

Explanation:

Ans. is ‘a’ i.e., Urgent IVP is indicated 

  • Approach to kidney should be transperitoneal to exclude the possibility of damage to other abdominal organs. Approach should not be Lumbar.
  • Aneurysm of renal artery is a rare complication -Bailey

Q. 2 All except one are correct regarding renal trauma ‑

 A

Observation is best

 B

IVP is indicated

 C

Exploration indicated in all cases

 D

Haematuria is a cardinal sign

Q. 2

All except one are correct regarding renal trauma ‑

 A

Observation is best

 B

IVP is indicated

 C

Exploration indicated in all cases

 D

Haematuria is a cardinal sign

Ans. C

Explanation:

Ans is ‘c’ ie. Exploration is indicated in all cases 

“Surgical exploration is needed in less than 10 percent of closed injuries and is indicated if either there a signs of progressive blood loss or there is an expanding mass in the loin.”- Bailey 25/e

  • More than 90 percent of all blunt renal injuries are managed conservatively.
  • An IVP is done urgently to assesss the damage to the kidney and to know the functioning of the other kidney.
  • Haematuria is the cardinal sign of a damaged kidney but it may not appear untill some hours after the injury. It is present in more than 95% of pts with renal injury. The degree of hematuria does not precisely correlate with the severity of injury.
  • Closed renal injury is usually extraperitoneal. The exception is seen occasionally in young children who have very little extraperitoneal fat. Their peritoneum is in close contact to the kidney and can tear with the renal capsule leaking blood and urine into the peritoneum.
  • Complications
  • Pararenal pseudohydronephrosis*
  • Hypertension* resulting from renal fibrosis may occur 3 months or more after injury. If is often refractory to medicines and nephrectomy may be necessary.
  • Aneurysm of the renal artery*.

Q. 3 Which does not happen in Unilateral Renal Trauma ‑

 A

Hypertension

 B

Uraemia

 C

Clot formation

 D

Perinephric haematoma

Q. 3

Which does not happen in Unilateral Renal Trauma ‑

 A

Hypertension

 B

Uraemia

 C

Clot formation

 D

Perinephric haematoma

Ans. B

Explanation:

Ans. is ‘b’ i.e., Uraemia 
Clinical features-

  • Hematuria is the most important sign of renal injury.
  • Loin bulge due to perinephric haemtoma.
  • Bruising of soft tissue in the loin.
  • Retroperitoneal haematoma –> abdominal distension.
  • systolic blood pressure ≤90 mmHg

Q. 4 Renal trauma is best treated by –

 A

Observation and supportive measures

 B

Early drainage of perirenal haematoma

 C

Heminephrectomy

 D

Nephrostomy

Q. 4

Renal trauma is best treated by –

 A

Observation and supportive measures

 B

Early drainage of perirenal haematoma

 C

Heminephrectomy

 D

Nephrostomy

Ans. A

Explanation:

Ans. is ‘a’ i.e., Observation and supportive measures 
Treatment-

  • Blunt trauma are treated conservatively
  • Penetrating injuries, small & major lacerations- surgical exploration.

Quiz In Between



Odontogenic Keratocyst

Odontogenic Keratocyst


                                ODONTOGENIC KERATOCYST

  • OKC arises from residual strands of epithelium from dental lamina.
  • Forms a cyst in the jaw in tooth bearing area.
  • Lined by keratinized squamous epithelium.
  • It is locally aggressive and high rate of recurrence
  • OKC –> ameloblastoma –> malignant lesion (SCC)

Clinical features-

  • Patient between 10- 40 years are affected.
  • Common in males.
  • Site 3rd molar tooth (posterior mandible)
  • Pre malignant jaw cyst

Treatment-

  • Osteotomy with enucleation with chemical cautery (Cornoy’s sign)
  • Recurrence rates for inadequate removed lesions can reach 60%.

Exam Important

Clinical features-

  • Patient between 10- 40 years are affected.
  • Common in males.
  • Site 3rd molar tooth (posterior mandible)
  • Pre malignant jaw cyst
Don’t Forget to Solve all the previous Year Question asked on Odontogenic Keratocyst

Module Below Start Quiz
 

Odontogenic Keratocyst

Odontogenic keratocyst

Q. 1 Which of the following jaw cyst is pre-malignant?

 A

Nasopalatine cyst

 B

Radicular cyst 

 C

Odontogenic keratocyst

 D

Dentigerous cyst

Q. 1

Which of the following jaw cyst is pre-malignant?

 A

Nasopalatine cyst

 B

Radicular cyst 

 C

Odontogenic keratocyst

 D

Dentigerous cyst

Ans. C

Explanation:

Ans. c. Odontogenic keratocyst

Odontogenic keratocysts are characterized by an epithelial lining that is parakeratinized and stratified. It is characterized by basal layer of neatly arranged, palisaded, columnar and cuboidal cells above which are several layers of squamous epithelium. This lining has a high mitotic rate and rarely may become dysplastic and develop into squamous cell carcinomas. “- Scott-Brown’s Otorhinolaryngology 

Nasopalatine duct cyst:

  • Relatively common non-odontogenic, developmental cyst
  • Arises from embryonic remnants of the nasopalatine duct
  •  Occurs in palatal midline behind the maxillary central incisors in the region of incisive canal
  • Usually asymptomatic; may be associated with salty discharge
  • Surgical enucleation via palatal flap is treatment of choice

Radicular cyst (Periapical cyst):

  • Most common type of jaw cyst
  • Develops at the apex of an infected, nonvital tooth
  • Bimodal incidence within the 3rd and 6th decade
  • Rarely seen in primary dentition
  • Usually presents as radioluscent lesion around the apex of a tooth root
  • Lined by proliferative epithelium of the non-keratinizing type with an intense inflammatory infiltrate
  • Normally resolve spontaneously if the infection in the associated tooth is controlled by root canal therapy
  • For persisting and larger lesion: Enucleation
  • Dentigerous Cyst:
  • 2nd Most common type of jaw cyst
  • Arises from unerupted teethQ
  • MC in lower 3rd molars
  • Cyst also contain unerupted teethQ
  • X-ray shows: Unilocular cyst or soap bubble appearanceQ
  • Treatment of choice: Enucleation

Odontogenic Keratocyst

  • Odontogenic keratocyst is locally aggressive and has a high rate of recurrenceQ.
  • Most often diagnosed in patients between 10-40 yearsQ.
  • Occur most commonly in males within the posterior mandible, particularly in the region of 3rd molar toothQ.
  • Radiographically present as well-defined unilocular or multilocular radiolucencies
  • Odontogenic keratocysts are characterized by an epithelial lining that is parakeratinized and stratified.
  • It is characterized by basal layer of neatly arranged, palisaded, columnar and cuboidal cells above which are several layers of squamous epithelium. This lining has a high mitotic rate and rarely may become dysplastic and develop into squamous cell carcinomaQ.

Treatment:

  • Aggressive and complete removal of the lesion
  • Recurrence rates for inadequately removed lesions can reach 60%Q

Quiz In Between



Pediatric burn injury

Pediatric burn injury


INTRODUCTION:

  • Burns and scalds account for 6% of peadiatric injuries.
  • The majority involve pre-school children,burns being most common between 1-2 yrs,flame burns bet 5-18 yrs.
  • Children have nearly 3 times BSA:BM ratio of adults.
  • Consequently greater fluid requirements and more evaporative water loss than adults.
  • Children
  • Burn that may appear partial thickness may instead be a full thickness burn.
BURNS:
Wounds caused by exposure to:
  • Excessive heat
  • Chemicals
  • Fire/steam
  • Radiation
  • Electricity
DEPTH OF BURN:
  • Partial thickness burn = involves epidermis
  • Deep partial thickness = involves dermis
  • Full thickness = involves all of skin
DEGREE OF BURN:

1st DEGREE BURN:

  • Involves only epidermis
  • Tissue will blanch with pressure
  • Tissue is erythematous and often painful
  • Involves minimal tissue damage
  • Sunburn

2nd DEGREE BURN:

  • Partial thickness burns 
  • Involve the epidermis and portions of the dermis 
  • Often involve other structures such as sweat glands, hair follicles, etc. 
  • Blisters and very painful 
  • Edema and decreased blood flow in tissue can convert to a full-thickness burn

3rd DEGREE BURN:

  • Referred to as fullthickness burns 
  • Charred skin or translucent white color 
  • Coagulated vessels visible 
  • Area insensate – patient still c/o pain from surrounding second degree burn area 
  • Complete destruction of tissue and structures

4th DEGREE BURN:

  • Involves subcutaneous tissue, tendons and bone
MAJOR BURNS:
  • PT and FTB with affected BSA>10% under 10yrs age. 
  • PT and FTB with affected BSA>20% over 10 yrs age. 
  • FTB with affected BSA>5%. 
  • PT or FTB involving face,hands,feet,perinium or major joints. 
  • PT or FTB involving an inhalational burn. 
  • PT or FTB involving an electrical or chemical burn.
BURNS EXTENT:
  • Burn extent is calculated only on individuals with second and third degree burns
  • Palmar surface = 1% of the BSA
MEASUREMENT CHARTS:
  • Rule of Nines: Quick estimate of percent of burn
  • Lund and Browder:
    • More accurate assessment tool
    • Useful chart for children – takes into account the head size proportion.
  • Rule of Palms: Good for estimating patches of burn wound
RULES OF NINES:
  • Head & Neck = 9%
  • Each upper extremity (Arms) = 9%
  • Each lower extremity (Legs) = 18%
  • Anterior trunk= 18%
  • Posterior trunk = 18%
  • Genitalia (perineum) = 1%
MANAGEMENT:

URGENT:

  • High flow o2 face mask with reservior bag.
  • Cervical collar (injury spine )
  • Cooling burn wound –cold running water for 15-20 min,avoid making pt hypothermic.
  • Prevent hypothermia
  • Insert min 2 peripheral cannula in unburnt skin
  • Fluid resusitatation
  • Insert urinary catheter in all pts>20% BSA.
  • Fast the pt and insert NG tube for all pts with>20% BSA,all intubated pts,head and neck burns,younger children >10%BSA.
  • Adequate analgesia-IV opoids.
  • Emergency wound management e.g.,cling film or clean non-adhesive dressing.
  • Escharotomy if indicated e.g., circumferential burns around limbs or trunk.

PARKLAND FORMULA:

  • 4 ml R/L x % burn x body wt. In kg. 
  • ½ of calculated fluid is administered in the first 8 hours 
  • Balance is given over the remaining 16 hours. 
  • Maintain urine output at 0.5 ml/kg/hr.  
  • If evidence of extensive tissue damage then aim for a higher UO 1-2 ml/kg/hr. 
  • Monitor sr electrolytes esp for hyponatremia. 
  • In younger children calculate the maintenance fluids and add this to the resusitation fluids

Surgeries and Dressings:

  • Escharotomy may be needed for circumferential burns to limbs,neck or trunk. 
  • Early surgical debridement of nectrotic tissue is preferred as early grafting is associated with improved outcome. 
  • Scrubbing of affected skin is also frequently undertaken. 
  • Blood loss during operative sessions can be large.

Escharotomy:

  • Circulation to distal limb is in danger due to swelling. 
  • Progressive loss of sensation / motion in hand / foot. 
  • Progressive loss of pulses in the distal extremity by palpation or doppler. 
  • In circumferential chest burn, patient might not be able to expand his chest enough to ventilate, and might need escharotomy of the skin of the chest.

Exam Important

  • According to Parkland formula, the initial orders for choice of fluid and rate of infusion should be Ringer’s lactate, 1250 ml/h for 71/2h
  • Burn injury with the body parts involved: face including scalp, both buttocks and circumferentially around both thighs TBSA 0.35
  • Burns in children assessed by Lund and Browder
  • Head and neck burns in infant constitute 18 of burns
  • Parkland formula for burns is for Ringer lactate

 

Don’t Forget to Solve all the previous Year Question asked on Pediatric burn injury

Module Below Start Quiz

Pediatric burn injury

Pediatric burn injury

Q. 1 A 3 year old child suffers from burn injury with the following body parts involved: face including scalp, both buttocks and circumferentially around both thighs. How much is TBSA involved? 

 A

0.25

 B

0.26

 C

0.35

 D

0.45

Q. 1

A 3 year old child suffers from burn injury with the following body parts involved: face including scalp, both buttocks and circumferentially around both thighs. How much is TBSA involved? 

 A

0.25

 B

0.26

 C

0.35

 D

0.45

Ans. C

Explanation:

Ans is ‘c’ i.e. 0.35 

Using Modified Lund-Browder chart:

Area

Percentage

 

Face

9

 

Scalp

9

 

Both buttocks

2.5 + 2.5 = 5

 

Both thighs circumferentially

3.5 x 2 + 3.5 x 2 =

15

Total body surface area

38

 

 [img id=10162]


Q. 2

Burns in children assessed by:     
AIIMS 13

 A

Rule of nine

 B

Lund and Browder

 C

Palmer surface method

 D

Hasse’s rule

Q. 2

Burns in children assessed by:     
AIIMS 13

 A

Rule of nine

 B

Lund and Browder

 C

Palmer surface method

 D

Hasse’s rule

Ans. B

Explanation:

Ans. Lund and Browder


Q. 3

Head and neck burns in infant constitute _____________of burns:          
Kerala 08

 A

9

 B

18

 C

24

 D

36

Q. 3

Head and neck burns in infant constitute _____________of burns:          
Kerala 08

 A

9

 B

18

 C

24

 D

36

Ans. B

Explanation:

Ans. 18

Quiz In Between
Q. 4

A 2-year-old child had burns on buttocks, both legs, face, neck and singeing of hair. Total surface area burnt:    
JIPMER 14

 A

27%

 B

37%

 C

45%

 D

55%

Q. 4

A 2-year-old child had burns on buttocks, both legs, face, neck and singeing of hair. Total surface area burnt:    
JIPMER 14

 A

27%

 B

37%

 C

45%

 D

55%

Ans. B

Explanation:

Ans. 37%


Q. 5

In a 6-year-old child with burns involving whole of head and trunk, the estimated body surface area involved:      
JIPMER 09

 A

44%

 B

48%

 C

55%

 D

58%

Q. 5

In a 6-year-old child with burns involving whole of head and trunk, the estimated body surface area involved:      
JIPMER 09

 A

44%

 B

48%

 C

55%

 D

58%

Ans. B

Explanation:

Ans. 48%


Q. 6

Parkland formula for burns is for:
Maharashtra 09; UP 09; Bihar 12

 A

Ringer lactate

 B

Glucose saline

 C

Normal saline

 D

25% dextrose

Q. 6

Parkland formula for burns is for:
Maharashtra 09; UP 09; Bihar 12

 A

Ringer lactate

 B

Glucose saline

 C

Normal saline

 D

25% dextrose

Ans. A

Explanation:

Ans. Ringer lactate

Quiz In Between


Atherosclerosis

Atherosclerosis


ATHEROSCLEROSIS

  • Atherosclerosis is an thickening & hardening muscular arteries which is characterised by soft gramous lipid cores (atheromatous plaque).
  • It is the commonest & most important arterial disease.
  • Most commonly affected are aorta, coronaries & cerebral arterial system.
  • Most commonly coronoary circulation affected is – Left anterior descending artery

Etiology

Pathogenesis-

  • Most widely accepted theory for atherosclerosis is inflammatory response to endothelial injury.
  • According to this hypothesis, atherosclerosis is a chronic inflammatory response of the arterial wall initiated by injury to endothelium.
  • Hyperlipidemia, hypertension, smoking can cause endothelial injury.
  • Foam cells are formed when macrophages & smooth muscle cells accumulated oxidised LDL.
  • Chlamydia Pneumoniae presents the strongest association with human atherosclerosis.

Morphological features-

1. Fatty streaks & Dots- are the earliest lesions composed of intimal collections of foamy macrophages & smooth muscle cells.

  • Prominent in the aorta (often in posterior wall)

2. Gelatinous lesions- develop in the intima of the aorta.

3. Artheromatous plaques (arthemaous lesions/ fibrous plaque)-

  • Most severely affected is the abdominal aorta.
  • Involves iliac, femoral, carotid, coronary & cerebral arteries.
  • Superficial luminal part of the fibrous cap (convex) composed by smooth muscle cells.
  • Cellular area under fibrous cap composed of macrophages, foam cells, lymphocytes.
  • Deeper central soft core consists of cholesterol clefts, fibrin, necrotic debris & lipid- laden foam cells.

4. Complicated plaques-

  • Calcification- occurs more commonly in advanced athermatous plaques.
  • Ulceration
  • Thrombosis- superimposed thrombi
  • Haemorrhage

Clinical features-

Major clinical effects of atheroscelrosis are-

  1. Heart (coronary artery disease, IMD, MI)
  2. Brain (stroke)
  3. Aorta (aneurysmal dilatation)
  4. Intestine (ischaemia, infarct)
  5. Lower extremities (gangrene)
  • Blood vessels affected by atherosclerosis- abdominal aorta (most commonly), Circle of Willis (least commonly affected)

Exam Important

  • Most commonly affected are aorta, coronaries & cerebral arterial system.
  • Most commonly coronoary circulation affected is – Left anterior descending artery

Etiology

Pathogenesis-

  • Most widely accepted theory for atherosclerosis is inflammatory response to endothelial injury.
  • According to this hypothesis, atherosclerosis is a chronic inflammatory response of the arterial wall initiated by injury to endothelium.
  • Hyperlipidemia, hypertension, smoking can cause endothelial injury.
  • Foam cells are formed when macrophages & smooth muscle cells accumulated oxidised LDL.
  • Chlamydia Pneumoniae presents the strongest association with human atherosclerosis.

Morphological features-

1. Fatty streaks & Dots- are the earliest lesions composed of intimal collections of foamy macrophages & smooth muscle cells.

  • Prominent in the aorta (often in posterior wall)

2. Gelatinous lesions- develop in the intima of the aorta.

3. Artheromatous plaques (arthemaous lesions/ fibrous plaque)-

  • Most severely affected is the abdominal aorta.
  • Involves iliac, femoral, carotid, coronary & cerebral arteries.
  • Superficial luminal part of the fibrous cap (convex) composed by smooth muscle cells.
  • Cellular area under fibrous cap composed of macrophages, foam cells, lymphocytes.
  • Deeper central soft core consists of cholesterol clefts, fibrin, necrotic debris & lipid- laden foam cells.

4. Complicated plaques-

  • Calcification- occurs more commonly in advanced athermatous plaques.
  • Ulceration
  • Thrombosis- superimposed thrombi
  • Haemorrhage
  • Blood vessels affected by atherosclerosis- abdominal aorta (most commonly), Circle of Willis (least commonly affected)
Don’t Forget to Solve all the previous Year Question asked on Atherosclerosis

Module Below Start Quiz

Atherosclerosis

Atherosclerosis

Q. 1 All will predispose to atherosclerosis except:

 A

Homocystinemia

 B

Fibrinogen

 C

Calcium

 D

Lipoprotein A

Q. 1

All will predispose to atherosclerosis except:

 A

Homocystinemia

 B

Fibrinogen

 C

Calcium

 D

Lipoprotein A

Ans. C

Explanation:

Q. 2

Atherosclerosis in the coronary circulation most commonly affects –

 A

Left anterior descending artery

 B

Left circumflex

 C

Right coronary

 D

All of the above

Q. 2

Atherosclerosis in the coronary circulation most commonly affects –

 A

Left anterior descending artery

 B

Left circumflex

 C

Right coronary

 D

All of the above

Ans. A

Explanation:

Ans. is ‘a’ i.e., Left anterior descending artery


Q. 3

In atherosclerosis, increased LDL in monocyte macrophage due to –

 A

LDL receptors on macrophage

 B

LDL receptors on macrophage

 C

Lipids in LDL’get oxidized

 D

Lipids in LDL’get oxidized

Q. 3

In atherosclerosis, increased LDL in monocyte macrophage due to –

 A

LDL receptors on macrophage

 B

LDL receptors on macrophage

 C

Lipids in LDL’get oxidized

 D

Lipids in LDL’get oxidized

Ans. C

Explanation:

Ans. is ‘c’ i.e., Lipids in LDL gets oxidized

Quiz In Between


Q. 4

All of the following are risk factors for atherosclerosis except :

 A Increased waist – hip ratio

 B

Hyperhomocysteinemia

 C

Decreased fibrinogen levels

 D

Decreased HDL levels

Q. 4

All of the following are risk factors for atherosclerosis except :

 A Increased waist – hip ratio

 B

Hyperhomocysteinemia

 C

Decreased fibrinogen levels

 D

Decreased HDL levels

Ans. C

Explanation:

Answer is C (Decreased fibrinogen levels)

Increased levels of .fibrinogen (and not decreased fibrinogen levels) are associated with increased risk of atherosclerosis.

  • Fibrinogen Levels

‘Fibrinogen levels correlate with coronary risk and provide information regarding coronary risk independent of lipoprotein profile. Elevated fibrinogen levels might promote a thrombotic diathesis’.

  • Waist Hip Ratio : This refers to a characteristic ‘male’ distribution of adipose tissue i.e. excess of fat in the abdomen compared with that in hips.

`An elevated waist/hip ratio has been associated with symptomatic cardiovascular disease and cerebrovascular disease in both men and women. – Pubmed (NCBI – website)

Hyperhomocvsteinemia and low HDL levels are known risk factors for Atherosclerosis (as depicted in the following table).

Major risk Factors for Atherosclerosis

  • Cigarette smoking
  • Hypertension (BP > 140/90mm/hg) or (on Antihypertensive medication)
  • Low HDL cholesterol
  • Diabetes mellitus
  • Family history of CHD
  • Age (Men > 45 years; Women > 55 years)
  • Life style risk factors Obeity (BMI > 30 kg/m2)

Physical inactivity Atherogenic diet

Emerging risk factors

  • Lipoprotein (a)
  • Homocystine             •
  • Prothrombotic factors (Fibrinogen)
  • Pro inflammatory factors
  • Impaired fasting glucose
  • Subcl inical atherogenesis

Q. 5 The amino acid which is associated with atherosclerosis is :

 A

Lysine

 B

Homocysteine

 C

Cysteine

 D

Alanine

Q. 5

The amino acid which is associated with atherosclerosis is :

 A

Lysine

 B

Homocysteine

 C

Cysteine

 D

Alanine

Ans. B

Explanation:

Answer is B (Homocysteine)

  • There is a strong positive correlation between atherosclerosis and circulating levels of Homocysteine’
  • Hyperhomocysteinemia has been most consistently linked with atherosclerosis and coronary thrombotic events
  • “Patient with clinical and angiographic evidence of coronary artery disease tend to have higher levels of plasma homocysteine. The relationship has not been extended to cerebrovascular and peripheral vascular disease”- CMDT
  • “A large body of literature suggests a relationship between hyperhomocysteinemia and coronary events. Several mutations in the enzymes involved in homocysteine accumulation correlate to thrombosis and (in some studies) coronary risk”
  • An increase of 5 micromol / L of homocysteine in serum elevates the risk of coronary artery disease by as much as cholesterol increase of 20 mg /dl.
  • Homocysteine interacts with lysyl residues of collagen interfering with collagen cross linking.
  • It forms homocysteine thiolactone, a highly reactive free radical which thiolates LDL particles.
  • These particles tend to aggregate, are endocytosed by macrophages and increase the tendency for atherogenesis.
  • Providing adequate quantity of pyridoxine, vitamin B12 and folic acid will keep homocysteine in blood in normal levels.
  • Maternal hyperhomocysteinemia is known to increase the chances of neural tube defects in foetus. So, high doses of folic acid are advised in pregnancy.

Q. 6 The most important modifiable risk factor for atherosclerosis is:

 A

Hyperlipidemia

 B

Diabetes mellitus

 C

Cigarette Smoking

 D

Hypertension

Q. 6

The most important modifiable risk factor for atherosclerosis is:

 A

Hyperlipidemia

 B

Diabetes mellitus

 C

Cigarette Smoking

 D

Hypertension

Ans. C

Explanation:

Answer is C (Cigarette Smoking)
Cigarette smoking is the single most important modifiable risk factor for atherosclerosis.

  • Smoking is the single most important modifiable risk factor for the development of Peripheral Artery Disease (PAD)
  • Smoking cessation is the single most important target Pr coronary artery disease (CAD) Prevention
  • Hypertension continues to be the most important of all modifiable risk factors for stroke

Quiz In Between


Q. 7 Which of the following statements about Atherosclerosis is true:

 A

Intake of Unsaturated Fatty Acids is associated with decreased risk

 B

Extent of lesions in veins is similar as that in arteries

 C

Thoracic Aorta is more commonly involved than abdominal aorta

 D

Hypercholesterolemia alone does not increase the risk of atherosclerosis per se

Q. 7

Which of the following statements about Atherosclerosis is true:

 A

Intake of Unsaturated Fatty Acids is associated with decreased risk

 B

Extent of lesions in veins is similar as that in arteries

 C

Thoracic Aorta is more commonly involved than abdominal aorta

 D

Hypercholesterolemia alone does not increase the risk of atherosclerosis per se

Ans. A

Explanation:

Answer is A (Intake of Unsaturated Fatty Acids is associated with decreased risk)

The maximal benefit is observed with Omega 3 Poly-unsaturated Fatty Acids, however Mono-unsaturated Fatty Acids also have consistent anti-atherosclerotic benefits and both Poly-unsaturated Fatty Acids (PUFA) and Mono­unsaturated Fatty Acids (MUFA) are considered Cardioprotective Fatty Acids.

Hypercholestoremia alone may increase the risk of Atherosclerosis

`Hyperlipidemia and more specifically hypercholesterolemia is a major risk factor lb,. atherosclerosis. Even in the absence of other factors, hypercholesterolemia is sufficient to stimulate lesion development’. – Robbins 8th/497 Extent of Athrosclerosis is more severe in arteries than in veins

Atherosclerosis is always severe in areas where pressure and velocity are high (as in arteries) in contrast to areas where pressure and velocity are low (as in veins).

‘Overall atherosclerosis is more severe in high-pressure arteries than in pulmonary arteries with lower blood pressure. It is least severe in veins where pressure and velocity are lowest’ – ‘Pan – Vascular Medicine’ by Topol (2002)/90 Abdominal Aorta is more commonly involved than Thoracic Aorta

`Abdominal Aorta is more commonly involved than Thoracic Aorta. Within the abdominal aorta lesions tend to be more prominent around the ostia’ – `Med Essentials’ (Kaplan Publishing) 2007/249

`In the systemic circulation  severity is accentuated in the abdominal aorta and large arteries of the lower limb where pulse wave reflection and summation effect elevate the pulse and systolic pressures. The disease is more severe in large  rather than small vessels indicating the importance of mural tension and Reynolds number both of which are proportional to radius increasing the likelihood and severity of effects of blood flow disturbance at arterial forks, junctions and curvatures’.- ‘Pan Vascular Medicine’


Q. 8

True about atherosclerosis ‑

 A

Chronic inflammatory disorder of vessel wall

 B

Not lead to complications of vessel wall

 C

Thoracic aorta more than abdominal aorta

 D

Atherosclerostic plaques do not demonstrate neovascularization

Q. 8

True about atherosclerosis ‑

 A

Chronic inflammatory disorder of vessel wall

 B

Not lead to complications of vessel wall

 C

Thoracic aorta more than abdominal aorta

 D

Atherosclerostic plaques do not demonstrate neovascularization

Ans. A

Explanation:

Ans. is ‘a’ i.e., Chronic inflammatory disorder of vessel wall

Facts about atherosclerosis

Is a chronic inflammatory and healing response of the arterial wall to endothelial injury.

Atherosclerosis progresses in the following sequence:

Endothelial injury and dysfunction → Accumulation of lipoproteins (mainly LDL) Monocyte adhesion to the endothelium, followed by migration into the intima and transformation into macrophages and foam cells → Platelet adhesion factor release from activated platelets, macrophages, and vascular wall cells → Smooth muscle cell proliferation, extracellular matrix production, and recruitment of T cells → Lipid accumulation both extracellularly and within cells (macrophages and smooth muscle cell).

In descending order, the most extensively involved vessels are the lower abdominal aorta, the coronary arteries, the popliteal arteries, the internal carotid arteries, and the vessels of the circle of Willis. In humans, the abdominal aorta is typically involved to a much greater degree than the thoracic aorta.



Q. 9

Foam cells in atherosclerosis contain lipid in the form of ‑

 A

Oxidized LDL

 B

Reduced LDL

 C

Oxidized VLDL

 D

Reduced VLDI

Q. 9

Foam cells in atherosclerosis contain lipid in the form of ‑

 A

Oxidized LDL

 B

Reduced LDL

 C

Oxidized VLDL

 D

Reduced VLDI

Ans. A

Explanation:

Ans. is ‘a’ i.e., Oxidized LDL

Morphology of atherosclerotic plaque

There are three major components of an atherosclerotic plaques :-

i) Cells : Smooth muscle cell and macrophages are the major cells with some contribution from foam cells (lipid-laden macrophages), and lymphocytes. Advanced atherosclerotic plaque may lack smooth muscles as smooth muscle cells undergo apoptosis.

ii) Extracellular matrix : Collagen, elastic fibers, proteoglycans.

iii) Lipids : Both intracellular and extracellular, with cholesterol and cholesterol ester being the major lipids.

Quiz In Between


Q. 10 Following are the modifiable risk factors of atherosclerosis except ‑

 A

Physical inactivity

 B

Obesity

 C

Diabetes

 D

Hypertension

Q. 10

Following are the modifiable risk factors of atherosclerosis except ‑

 A

Physical inactivity

 B

Obesity

 C

Diabetes

 D

Hypertension

Ans. B

Explanation:

Ans. is ‘b’ i.e., Obesity


Q. 11

True about the basic structure of atherosclerosis plaque is ‑

 A

Concave part formed by fibrous cap

 B

Convex part formed by tunica media of the vessel

 C

Convex part formed by fibrous cap

 D

Necrotic core contains collagen, elastin and proteoglycans

Q. 11

True about the basic structure of atherosclerosis plaque is ‑

 A

Concave part formed by fibrous cap

 B

Convex part formed by tunica media of the vessel

 C

Convex part formed by fibrous cap

 D

Necrotic core contains collagen, elastin and proteoglycans

Ans. C

Explanation:

Ans. is ‘c’ i.e., Convex part formed by fibrous cap

  • The convex part is formed by the fibrous cap, which consists of smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin and proteoglycans.
  • The central necrotic core is formed of cell debris, cholesterol crystals, foam cells and calcium.
  • The concave part is formed by the tunica media of the vessel

Q. 12 Atherosclerosis initiation by fibroblast plaque is mediated by injury to ‑

 A

Smooth muscle

 B

Media

 C

Adventitia

 D

Endothelium

Q. 12

Atherosclerosis initiation by fibroblast plaque is mediated by injury to ‑

 A

Smooth muscle

 B

Media

 C

Adventitia

 D

Endothelium

Ans. D

Explanation:

Ans. is ‘d’ i.e., Endothelium

  • The most acceptable hypothesis for the pathogenesis of atherosclerosis is “the response to injury hypothesis”.
  • According to this hypothesis, atherosclerosis is a chronic inflammatory response of the arterial wall initiated by injury to endothelium.

Pathogenesis of atherosclerosis

  • Following stages occurs in the pathogenesis of Atherosclerosis:
  • Endothelial injury
  • Earliest stages of the development of atherosclerosis are mediated by the inflammatory cascade.
  • Inflammation mediated injury to endothelium is the cornestone in the development of atherosclerosis.
  • After injury, endothelium is activated and there is increased expression of adhesion molecule-VCAM-1 and
  • there is increased permeability to endothelium.
  • TNF is the major cytokine to induce this expression.

Migration of leukocytes

  • When VCAM-1 is expressed on endothelium, leukocytes adhere to the endothelium.
  • Leukocytes than cross the endothelial barrier and begin to accumulate in subendothelial intimal space.
  • Macrophages engulf LDL cholesterol and form foam cells → formation of earliest lesion, i.e. fatty streak.
  • Macrophages also form oxygen free radicals that cause oxidation of LDL to yield oxidized LDL (modified LDL).
  • Smooth muscle cell migration and proliferation
  • Inflammatory cells in subendothelial intimal space secrete cytokines, mainly PDGF, TGF-ct and FGF which cause migration of smooth muscle cells from media to subendothelial intimal space as well as their proliferation.

Maturation of plaque

  • Smooth muscle cells synthesize extracellular matrix (especially collegen) and convert a fatty streak into a mature fibrofatty atheroma, and contribute to the progressive growth of atherosclerotic lesions.

Q. 13 Identify this lesion in the formation of Atherosclerosis.

 A

Early lesion

 B

Fully developed Atheromatous Plaque

 C

Complicated Plaque

 D

None of the above.

Q. 13

Identify this lesion in the formation of Atherosclerosis.

 A

Early lesion

 B

Fully developed Atheromatous Plaque

 C

Complicated Plaque

 D

None of the above.

Ans. C

Explanation:

Ans:C.)Complicated Plaque
Schematic Evolution of Lesions in Atherosclerosis.
[img id=6454] 
MORPHOLOGIC FEATURES

1. FATTY STREAKS AND DOTS. 

  • Grossly, the lesions may appear as flat or slightly elevated and yellow.
  • They may be either in the form of small, multiple dots, about 1 mm in size, or in the form of elongated, beaded streaks.
  • Microscopically, fatty streaks lying under the endothelium are composed of closely-packed foam cells, lipid containing elongated smooth muscle cells and a few lymphoid cells. 

2. GELATINOUS LESIONS.

  • They are round or oval, circumscribed grey elevations, about 1 cm in diameter.
  • Microscopically, gelatinous lesions are foci of increased ground substance in the intima with thinned overlying endothelium.

3. ATHEROMATOUS PLAQUES.

  • A fully developed atherosclerotic lesion is called atheromatous plaque, also called fibrous plaque, fibrofatty plaque or atheroma.
  • Grossly, atheromatous plaques are white to yellowish white lesions, varying in diameter from 1-2 cm and raised on the surface by a few millimetres to a centimetre in thickness.
  • Cut section of the plaque reveals the luminal surface as a firm, white fibrous cap and a central core composed of yellow to yellow-white, soft, porridgelike material.
  • Microscopically, the following features are invariably present :
  • Superficial luminal part of the fibrous cap is covered by endothelium, and is composed of smooth muscle cells, dense connective tissue and extracellular matrix containing proteoglycans and collagen.
  • Cellular area under the fibrous cap is comprised by a mixture of macrophages, foam cells, lymphocytes and a few smooth muscle cells which may contain lipid.
  • Deeper central soft core consists of extracellular lipid material, cholesterol clefts, fibrin, necrotic debris and lipid laden foam cells.

4. COMPLICATED PLAQUES.

  • Various pathologic changes that occur in fully-developed atheromatous plaques are called the complicated lesions. 
  • These changes include calcification, ulceration, thrombosis, haemorrhage and aneurysmal dilatation.

Quiz In Between



Mitochondrial DNA

Mitochondrial DNA


Mitochondrial DNA (mtDNA)

  • It is a separate genome located in the cytoplasm of nearly all eukaryotic cells
  • Is closede circular, double-stranded, and composed of heavy (H) and light (L) chains or strands.
  • Contains 16,569 bp.
  • Encodes 13 protein subunits of the respiratory chain (of a total of about 67) –
  1. Seven subunits of NADH dehydrogenase (complex I) and Cytochrome b of complex III
  2. Three subunits of cytochrome oxidase (complex IV)
  3. Two subunits of ATP synthase
  • Encodes large (16S) and (12S) mt ribosomal RNAs
  • Encodes 22 mt tRNA molecules
  • Genetic code differs slightly from the standard code –
  1. UGA (standard stop codon) is read as Trp.
  2. AGP and AGG (standard codons for Arg) are read as stop codons,
  • Contains very few untranslated sequences.
  • Nemaline myopathy results due to mutations in mt- DNA
  • Heteroplasmy is the presence of mixture of more than one type of an organelle genome (mt- DNA) within a cell or individual.
  • High mutation rate (5 to 10 times that of nuclear DNA).
  • Comparisons of mtDNA sequences provide evidence about evolutionary origins of primates and other species.
  • High mutation rate occurs due to point mutation and large scale rearrangements.
  • mitochondrial DNA contains no (or very few) introns (i.e. untraslated sequences).

Mitochondrial DNA is always maternally inherited.

  1. Important mitochondrial diseases are mitochondrial encephalomyopathy with lactic aciilosis and stroke like episodes (MELAS),
  2. leber hereditary optic neuropathy, myoclonic epilepsy with ragged-red fibers, leigh syndrome, Pearson syndrome, kearns-sajre syndrome,
  3. chronic progressive external ophthalmoplegia and NARP (neurogenic weakness with ataxia & retinitis pigmentosa).
  • All children from affected mother will inherit the disease but it will not be transmitted from an afiected father to his children

Exam Important

  • Is closede circular, double-stranded, and composed of heavy (H) and light (L) chains or strands.
  • Contains 16,569 bp.
  • Encodes 13 protein subunits of the respiratory chain (of a total of about 67)
  • Nemaline myopathy results due to mutations in mt- DNA
  • Heteroplasmy is the presence of mixture of more than one type of an organelle genome (mt- DNA) within a cell or individual.
  • High mutation rate (5 to 10 times that of nuclear DNA).
  • Comparisons of mtDNA sequences provide evidence about evolutionary origins of primates and other species.
  • High mutation rate occurs due to point mutation and large scale rearrangements.
  • mitochondrial DNA contains no (or very few) introns (i.e. untraslated sequences).
  • Mitochondrial DNA is always maternally inherited.
  • All children from affected mother will inherit the disease but it will not be transmitted from an afiected father to his children
Don’t Forget to Solve all the previous Year Question asked on Mitochondrial DNA

Module Below Start Quiz

Mitochondrial DNA

Mitochondrial DNA

Q. 1 Mitochondrial DNA is:

 A

Closed circular

 B

Nicked circular

 C

Linear

 D

Open circular

Q. 1

Mitochondrial DNA is:

 A

Closed circular

 B

Nicked circular

 C

Linear

 D

Open circular

Ans. A

Explanation:

Mitochondrial DNA is a closed circular double helix molecule which is transmitted maternally and is found within cells in multiple copies.
It contains 37 genes. All of these genes are essential.

Ref: Ganong’s Review of Medical Physiology, 22nd Edition, Page 10

 


Q. 2

All of the following states are TRUE regarding mitochondrial DNA (mtDNA) disease, EXCEPT:

 A

mtDNA contains only 37 genes

 B

Cause Leber hereditary optic neuropathy

 C

Mitochondrial genome is maternally transmitted

 D

Heteroplasmy is a feature of mtDNA

Q. 2

All of the following states are TRUE regarding mitochondrial DNA (mtDNA) disease, EXCEPT:

Cause Leber hereditary optic neuropathy

 A

mtDNA contains only 37 genes

 B
 C

Mitochondrial genome is maternally transmitted

 D

Heteroplasmy is a feature of mtDNA

Ans. D

Explanation:

All human cells contain two genomes: one in the nucleus and one in the mitochondria. 

  • The mitochondrial genome contains only 37 genes
  • Genome is maternally transmitted. 
The ratio of genetically aberrant to normal mitochondria transmitted can vary during mitosis and through generations—a situation known as heteroplasmy. People with entirely faulty mitochondria (homoplasmy) or a large proportion of faulty mitochondria may develop a mtDNA disease. 
 
These are clinically heterogeneous but usually severe diseases resulting from defects in energy production and include deafness, blindness, diabetes, loss of skills, and heart and liver failure. About 1 in 400 people has a maternally inherited mtDNA mutation.
 
Ref: Ethics of mitochondrial gene replacement: from bench to bedside, Annelien L Bredenoord ; BMJ 2010;341:c6021

Q. 3 True about mitochondrial DNA

 A

UGA codes for tryptophan

 B

Codes for 13 protein

 C

Circular double stranded DNA

 D

All

Q. 3

True about mitochondrial DNA

 A

UGA codes for tryptophan

 B

Codes for 13 protein

 C

Circular double stranded DNA

 D

All

Ans. D

Explanation:

A, B,C i.e. UGA codes for tryptophan, Codes for 13 protein, Circular double stranded DNA, Mitrochondrial disease occur due to Point Mutations and Large-Scale Rearrangements

Quiz In Between


Q. 4

Mitochondrial DNA is:

 A

Paternally inherited

 B

Maternally inherited

 C

Horizontal inheritance

 D

Vertical inheritance

Q. 4

Mitochondrial DNA is:

 A

Paternally inherited

 B

Maternally inherited

 C

Horizontal inheritance

 D

Vertical inheritance

Ans. B

Explanation:

B i.e. Maternally inherited


Q. 5

Mitochondrial DNA (mt- DN(A) is known for all except –

 A

Maternal inheritance

 B

Heteroplasmy

 C

Leber hereditary optic neuropathy is the prototype

 D

Nemaline myopathy results due to mutations in mt- DNA

Q. 5

Mitochondrial DNA (mt- DN(A) is known for all except –

 A

Maternal inheritance

 B

Heteroplasmy

 C

Leber hereditary optic neuropathy is the prototype

 D

Nemaline myopathy results due to mutations in mt- DNA

Ans. D

Explanation:

Ans. is ‘d’ i.e., Nemaline myopathy results due to mutations in mt- DNA

o Nemaline myopathy is not a mitochondria] disorder.

o Mitochondrial DNA is always maternally inherited.

o Heteroplasmy is the presence of mixture of more than one type of an organelle genome (mt- DNA) within a cell or individual. It is a factor for the severity of mitochondrial disease, since every eukaryotic cell contains many hundreds of copies of mt- DNA; it is possible and indeed very frequent for mutations to affect only some of the copies, while the remaining ones are unaffected.


Q. 6 Function of mitochondrial DNA ‑

 A

Encodes proteins of cell membrane

 B

Encodes proteins of respiratory chain

 C

Helps in cell replication

 D

Formation of rRNA

Q. 6

Function of mitochondrial DNA ‑

 A

Encodes proteins of cell membrane

 B

Encodes proteins of respiratory chain

 C

Helps in cell replication

 D

Formation of rRNA

Ans. B

Explanation:

 
Human mitochondria contain two to ten copies of a small circular double-stranded DNA molecule that makes up approximately 1% of total cellular DNA.
The majority of the peptides in mitochondria (about 54 out of 67) are coded by nuclear genes.
The rest are coded by genes found in mitochondrial (mt) DNA
This mtDNA codes for mt ribosomal and transfer RNAs and for 13 proteins that play key roles in the respiratory chain.

Quiz In Between



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