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Uworld Flashcards

1
Q

Side effects of Diltiazem (non-dihydropyridine CCB)

A

Constipation, oedema, hypotension

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2
Q

Medications causing constipation

A

Ondansetron, granisterone, verapamil, diltiazem, iron, aluminium,diphenhydramine, amytriptyline, diclyclomine, haloperidol, morphine, oxycodone, loperamide.

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3
Q

MOA of constipation caused by CCB

A

slow contraction of colonic smooth muscle

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4
Q

MOA of constipation in diabetic neuropathy

A

impairement of gastrocolic reflex

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5
Q

MOA of constipation in elderly/neurologic conditions?

A

dyssenergic defecation

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6
Q

Symptoms of sigmoid volvulus

A

abdominal pain, nausea, vomitting, bowel obstruction

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7
Q

How are pigment gall stones formed

A

increased efflux of bilirubin into bile

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8
Q

How are gall stones formed in ileal disease like Chrons

A

altered enterohepatic circulation

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9
Q

How are pigment gall stones formed

A

increased efflux of bilirubin into bile

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10
Q

How are gall stones formed in ileal disease like Chrons

A

altered enterohepatic circulation

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11
Q

Cause of diabetic diarrhea that persists at night (even with fasting) and day

A

autonomic neuropathy causing disordered motility of small bowel and colon and increased secretions

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12
Q

Risk factors for diabetic diarrhea

A

Impaired glucose control and vascular (obesity and HT)

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13
Q

Cause of diabetic diarrhea that persists at night and day

A

disordered motility of small bowel and colon

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14
Q

Risk factors for diabetic diarehea

A

Impaired glucose control and vascular (obesity and HT)

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15
Q

Diarrhea in exocrine pancreatic insufficiency

A

steatorrhea

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16
Q

What nutrient deficiency is seen with PPI

A

calcium, iron, magnesium and vitamin B12

PPI improve lipase as acid inactivates lipase

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17
Q

MOA of constipation in pregnancy

A

progesterone causes decreased colonic smooth muscle activity

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18
Q

Pathophysiology of ADH/RAS in cirrhosis

A

cirrhosis causes vasodilatation, reduces blood flow, activates RAS and increase ADH, increases renal Na reabsorption (hence decreasing urine sodium). This increases TBW but due to third spacing they are intravascularly depleted causing hypervolumic hypernatremia in advanced cirrhosis

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19
Q

MOA of constipwtion in pregnancy

A

progesterone causes colonic smooth muscle activity

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20
Q

Effects of pregnancy on GI tract

A

progesterone decreases LE tone-GERD
estrogen increases cholesterol secretion in bile, progesterone decreases GB motility-GB stones
Gravid uterus mechanical effect-flatulence
gravid uterus increase mechanical pressure-hemorrhoids

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21
Q

constipation after a traumatic vaginal delivery MOA

A

defecatory dysfunction, inablity to relax pelvic floor muscles
Rectoceles can occur after multiple vaginal deliveries

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22
Q

Most common cause of hepatic abscess in the US

A

Staph aureus by hematogenous route

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23
Q

Bacteria causing ascending cholangitis/hepatic abscess from direct invasion of nearby source?

A

Gm negative enteric bacilli like E coli, Kleibsiella, enterococcus

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24
Q

How does Entameoaba histolytica cause hepatic abscess

A

ascending from the colon through portal venous system

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25
Q

How does enteric bacteria cause hepatic abscess?

A

ascending through the biliart tract (ascending cholangitis), portal vein pyemia, direct invasion from an adjacent area (cholecystitis)

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26
Q

Pathophysiology of GERD

A

decreased LES tone, disruption of GE junction like in hiatal hernia

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27
Q

Complications of GERD

A

stricture, erosive esophagitis, Barrett esophagus

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28
Q

Food getting stuck in esophagis?

A

Stricture

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29
Q

Indectious esophagitis generally in immunocompromised organism?

A

Candida, CMV, HSV

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30
Q

New onset odynophagia in the setting of chronic GERD?

A

erosive esophagitis with esophageal ulcers

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31
Q

Enterocytes with foamy cytoplasm?

A

Abetalipoprotenemia due to accumulation of lipids

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32
Q

Nausea, fever, anorexia, hypotension after a surgery. What is it?

A

Inhaled anesthetic like halothane causing acute liver injury.

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33
Q

What kind of liver injury does halogenated anesthetics cause?

A

Hepatocellular injury, ranging from asymptomatic rise in liver enzymes to fulminant hepatitis. Liver shrunken on biospy.

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34
Q

Lab feautures of anesthtic induced hepatotoxicity?

A

Elevated aminotransferase, prolonged PT, leukocytosis and eosinophilia. Note distended abdomen veins and palmar erythema are features of end stage liver disease. Not acute liver toxicity.

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35
Q

Most common cause of acute cholecystitis?

A

Obstruction of the cystic duct.

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36
Q

complications of cholecystitis?

A

gangrene, perforation, pericholecystitis, generalised peritonitis.

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37
Q

imaging of choice for cholecystitis?

A

ultrasound

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38
Q

characteristics of cholecystitis on HIDA scan?

A

Gall bladder will not be visualised due to obstruction.

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39
Q

Characteristics of cholecystitis on ultrasound?

A

gall bladder thickening, pericholecystic fluid and positive sonographic Murphys sign

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40
Q

short gastric veins drain blood from ?

A

fundus to splenic vein

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41
Q

What causes splenic vein thrombosis and hence gastric varices?

A

Pancreatic inflammation like chronic pancreatitis, pancreatic cancer.

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42
Q

How do the azygous vein drain

A

drains blood from the esophageal vein into the SVC. Also provides collateral circulation between SVC and IVC and hence becomes enlarged with caval obstruction.

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43
Q

Blockage of superior mesentric vein cause varices where?

A

LOWER stomach, not upper regions. Remember SMV drains blood from the lower stomach and small intestine.

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44
Q

cause of atresia of jejunum, ileum and colon?

A

vascular occlusion

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45
Q

Where is apple peel atresia seen?

A

in superior mesenteric artery obstruction. Apple peel: blind ending proximal jejunum, a length of absent bowel and mesentery, a terminal ileum spiraled around an ileocolic vessel.

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46
Q

when is 5HT3 used for nausea?

A

visceral nausea like gastroenteritis, chemotherapy and anesthetics

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47
Q

When are dopamine antagonist used for nausea?

A

central nausea like migraines

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48
Q

When are H1 antagonists and muscarinic acetylcholine receptor antagonists used for nausea?

A

vestibular nausea like motion sickness

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49
Q

when is somatostatin receptor agonist (octreotide) used?

A

carcinoid and VIPOma diarrhea

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50
Q

Pathophysiology of umbilical hernia?

A

incomplete closure of abdominal muscles; defect in linea alba

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51
Q

when to treat umbilical hernia?

A

elective surgery after the age of 5

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52
Q

pathophysiology of ompahlocele and gastrotrichisis

A

failure of extraembryonic gut to return to the abdominal cavity

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53
Q

risk factors for chronic pancreatitis?

A

alchol, recurrent acute pancreatitis, smoking

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54
Q

What does chronic pancreatitis cause

A

endoceine (insulin) and exocrine(lipase, elastase, amylase, trpysin and chymotrypsin) deficiency

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55
Q

clinical features of chronic pancreatitis

A

steatorrhea, low fecal elastase, positive sudan staining, elevated hemoglobin HbA1c

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56
Q

what happens to pancreatic bicarb production in chronic pancreatitis?

A

due to destruction, pancreatic bicarb production decreases

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57
Q

characteritiscs of celiac disease

A

villous atrophy, abdominal pain, can have steatorrhea, iron deficiency anemia.

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58
Q

chronic infection with which 2 viruses cause hepatocellular carcinoma HCC?

A

Hep B and Hep C. Ongoing infection leads to increased hepatocyte turnover, generation of local inflammatory cytokines which can result in genetic mutations that lead to malignant transformation.

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59
Q

mechanism hoe HBV cause HCC

A

Intergration of HBV DNA into the host genome, production of oncogenic viral proteins called HBx that is assocaited with cellular growth, also aftects p%# which is tumor suppresor

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60
Q

Which viruses intergrate into host genome?

A

Hep B, HPV

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61
Q

How are calcifications formed in chronic alchoholic pancreatitis.

A

Protenaceous material precipitate to form ductal plugs, which then calcifies.

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62
Q

How does chronic pancreatits cause diarrhea?

A

digestive enzyme deficiency

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63
Q

Where is bile malabsorption seen?

A

ileal resection, chrohns

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64
Q

How do gastrinomas cause diarrhea/malabsorption?

A

hypersecretion of HCl that cause deactivation of digestive enzymes

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65
Q

how does celiac disease cause malabsoption?

A

immune mediated enteropathy

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66
Q

Gastric relation in systemic mastocytosis

A

abnormal proliferation of mast cells that secrete histamine, That causes hypersecretion of gastric acid by pareital cells in the stomach as well as hypotension, flushing and pruritis

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67
Q

What stimulates gastric acid secretion?

A

Histamine increases cAMP, acetylcholine increases intracellular calcium, gastrin binds to cholecystokinin B and increases intracellular calcium

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68
Q

Mast cell proliferation associated with which mutation

A

Mutation in KIT receptor tyrosine kinase

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69
Q

where is gastric hypomobility seen?

A

diabetes, uremia and hypothyroidism

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70
Q

pancreatic endocrine tumor secretions?

A

gastrin (ZE) insulin, glucagon, somatostatin(diarrhea, cholelitiasis, hyperglycemia), VIP(watery diarrhea, hypokalemia, acholyrydia.

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71
Q

Acid base changes in diarrhea?

A

low Ph, low paCO2 and low bicarb

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72
Q

Causes of anion gap metabolic acidosis

A

MUDPILES

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73
Q

Causes of non anion gap metabolic acidosis

A

HARDASS

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74
Q

Causes of metabolic alkalosis

A

nasogastric suctioning or severe vomitting, diuretic overuse, primary hyperaldosteronism

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75
Q

causes of respiratory acidosis (hypoventilation)

A

CNS depression (opoid overuse), OHS, nuromuscular weakness, COPD

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76
Q

Causes of respiratory alkalosis (hyperventilation)

A

Acute V/Q mismatch (PE, pneumonia), anxiety, inadequate pain control, high altitude, pregnancy

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77
Q

Changes when a patient with SIADH is given Vaptans (tolvaptan) or V2 antagonistsVasopressin?

A

Plasma osmolarity and urine output increases, serum sodium no change. No effect on Na and K excretion.

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78
Q

Changes in SIADH prior to treatment?

A

low serum osmolarity, low serum Na, low urine output, high urine osmolarity

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79
Q

CHanges by thiazides?

A

renal excfretion of Na and water (hence increase urine output), decreased plasma osmolarity (hyponatermia)

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80
Q

Changes due to dehydration?

A

dehydration causes increased plasma osmolarity, activates RAS, increas ADH (reduces urine output), and sodium excretion (due to alsosterone)

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81
Q

Changes due to mannitol?

A

increases plasma osmolarity and inhibits water reabsorption in the renal tubules. Sodium excretion is increased due to solvent drag.

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82
Q

Which poisoning in a pt with altered mental status, tachypnea and anion gap?

A

Aspirin (salicylate) poisoning

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83
Q

Symptoms of aspirin poisoning?

A

tinnitus, hyperventilation, nausea and vomitting. Uncoupling of oxydative phosphorylation leads to hyperthermia and anaerobic respiration and hence lactic acidosis. ALtered mental status due to direct effcet on CBS and neuroglycopenia.

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84
Q

Symptoms of ethanol intoxication

A

slurred speech, respiratory depression, nystagmus, decfreased cordination, CNS depression.

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85
Q

Symptoms of carbon monoxide posisoning?

A

many people in household flu like symptoms, headaches and altered mental status.

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86
Q

causes of hypophosphatemia?

A

internal redistribution {increased insulin secretion-refeeding, acute respiratory alkalosis-stimulates glycolysis, hungry bone syndrome-after parathyroidectomy}
decreased intestinal absorption {chronic poor intake, aluminium or Mg antacids since they bind phosphorus, steattorhea}
increased urinary excretion {primary and secondary hyperparathyroidism, vitamin D Deficiency, primary renal phosphate wasting, fanconi}

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87
Q

Mechanism of hypophosphatemia in refeeding?

A

redistribution of phosphorus from the serum into the muscle and hepatic cells in an effort to maintain cellulat energy metabolism (ATP production)

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88
Q

Hungry bone syndrome?

A

2-4 days after parathyroidectomy. Hypocalcemia and hypophosphatemia. Most prominent tetany.

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89
Q

Causes of SIADH?

A

CNS disturbances (stroke, h`age, trauma), meds(carbamazapine, SSRIs, NSAIDs), lung disease(pneumonia), malignancy (small cell lung cancer)

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90
Q

Clinical findings of SIADH?

A

nausea, forgetfullness (mild hyponatremia), seizures, coma (severe hyponatremia), euvolemia (moist mucous membranes, no odema, no JVD)

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91
Q

SE of canagliflozin?

A

increases urinary glucose excretion. Linked to UTI and hypotension.

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92
Q

Recurrent pyelonephritis and scarring on US?

A

reflux nephropathy. If uncorrected scarring (upper and lower pole) can lead to secondary hypertension.

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93
Q

Symptoms of ADPKD?

A

In adulthood, hematuria, HT and parenchymal cysts on US

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94
Q

Symptoms of multicystic dysplastic kidney?

A

multiple non communicating cyst with intervening dysplastic tissue. Early severe renal insufficiency.

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95
Q

symptoms of PUV?

A

b/l hydronephrosis and calcyleal dilatation. Only in males due to malformation of the Wolffian duct.

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96
Q

What happens in nephrogenic DI

A

serum osm high (same in central DI), urine osm after water deprivation low (same in central DI), urine osm after desmopressin administration no change (vs in central DI, urine osm will increase after desmopressin)

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97
Q

What happens in primary polydypsia?

A

serum osm low, urine osm after water deprivation increased, urine osm with desmopressin no change

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98
Q

mechanism in HUS?

A

bacterial toxins injure blood vessels, cause platelet aggregation and microthombi in blood vessels

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99
Q

features of HUS

A

bloody diarrhea, hemolytic anemia with schistocytes, thrombocytopenia, acute kidney injury

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100
Q

mechanism in PSGN?

A

immune response against streptococcal antigens that deposit in the glomerulus

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101
Q

mechanism in HSP

A

IgA immune complex deposition in the small blood vessel

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102
Q

mechanism in Kawasaki

A

vasculitis in medium sized arteries

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103
Q

mechanism in DIC

A

widespread activation of coagulation cascade

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104
Q

Why does post op urinary retension occur?

A

decfeased micturation reflex activity, decreased contractility of the bladder detrusor, increased vescical sphincter tone

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105
Q

Rx of post op urinary retension?

A

muscarinic agonist (bechanichol) or a alpha 1 blocking agent

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106
Q

Rx of bladder outlet obstruction sec to prostate hypertrophy

A

Finasteride, 5 alpha reductase inhibitor

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107
Q

Rx of urge incontinence?

A

Oxybutynin which is an antimuscarinic

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108
Q

Mechanics at high altitude?

A

Low piO2 leads to hypoxemia with hyperventilation and respiratory alkalosis.The hypoxemia and alkalemia cause symptoms like headache, fatigue, lightheaded. Kidney respons by creating metabolic acisosis by decreasing bicarb resabsoption and incfreasing erythropoeitin secretion. Alkalosis causes legft shift in Hb dissocoation curve.

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109
Q

What happens to renal dynamics in hypovolemia?

A

Decreased RPF, decreased GFR, increase FF

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110
Q

Kidney biospy of intimal thickening, luminal narrowing of the renal arterioles with glomerular sclerosis seen in what?

A

Hypertensive nephrosclerosis

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111
Q

Pathologic hypertensive changes in kidney?

A

medial hypertrophy, fibrointimal proliferation in the renal arteriole. There is also hylanie arteriosclerosis and glomerulosclerosis.

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112
Q

Urinalysis in hypertensive nephrosclerosis?

A

Proteinuria in advance disease, otherwise normal

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113
Q

Pathologic findings in analgesic nephropathy

A

papillary necrosis, tubolointerstitial nephritis

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114
Q

Pathologic findings in fibromuscular dysplasia?

A

fibromuscular ridges alternating with areas of anuerymal dilatation affecting the main renal artery

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115
Q

Renal histology in hepatitis C

A

diffuse thickening of the glomerular basement membrane without glomerular hypercellularity

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116
Q

Renal histology in multiple myeloma?

A

light chain cast nephropathy

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117
Q

What causes hemoptysis in cystic fibrosis?

A

bronchiectasis which stimuleates bronchial artery hypertrophy

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118
Q

What can cause life threatening hemoptysis?

A

bleeding from high pressure bronchial system not low grade pulmonary system

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119
Q

Where do you see large PaO2 gradient between alveoli and pulmonary venous blood and normal pCO2?

A

diffusion impairement (emphysema, pulmonary fibrosis)

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120
Q

What happens in normal arteriolar ventilation?

A

alveolar and pulmonary capillary pO2 reaches equilibrium at 104.

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121
Q

Where is intrapulmonary shunting seen?

A

When alveoli are filled with fluid (pneumonia, pulmonary oedema), or collapse atelectasis and alveolar ventilation is essentially zero.

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122
Q

dynamics in intrapulmonary shunting?

A

alveolar paO2 equilibrates wigth venous blood at 40 when alveolar ventilation is zero.

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123
Q

What happens in poor alveolar ventilation (hypoventilation)?

A

no gradient is created

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124
Q

Landmarks for thorcaocentesis?

A

between 6th and 8th in midclavicular line, between 8th and 10th in the midaxillary line and 10th and 12th paravertebral line

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125
Q

what happens if thoracocentesis needle is inserted lower than 9th rib?

A

damage to intraabdominal structures

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126
Q

how should throcacocentesis be performed to avoid damage to the intercostal vessels?

A

above the upper border of the rib

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127
Q

prolonged pauses in airflow despite normal thoracic and diaphragmatic activity?

A

OSA. Apneic episodes may result in hypoxia and hypercapnea.

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128
Q

breathing pattern in Chene sttoke heart failure?

A

a cyclical pattern in which apnea is followed by gradually increasing then decreasing tidal volumes (cresendo decresendo) until the next apneic period.

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129
Q

breathing pattern in redulced lung compliance?

A

rapid shallow breathing, to restore minjute ventilation and minimize work of breathing

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130
Q

breathing pattern in neruromuscular weakness?

A

reduced thoracic and diaphragmatic muscle activity with rapid shallow breathing

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131
Q

breathing activity in diabetic ketoacidosis Kussumal breathing?

A

deep rapid breathing associated with increased thoracic and diaphragmatic activity

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132
Q

Pathology of granulomas in sarcoidosis?

A

non caseating granulomas (non-necrotic aggregates of epitheloid macropahges and multinucleated giant cells)

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133
Q

clinical features of sarcoidosis?

A

lungs (reticular, nodular infiltrates), lymph nodes(hilar LN), skin (erythematous rash), eyes (anterior uveitis), pulmonary symptoms(cough, dypnea, SOB0, constituional (fever, weight loss, fatigue, night sweats, arthalgia)

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134
Q

Pathology in Hodgkin lymphoma?

A

Reed sternburg cell

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135
Q

pathology of sqamous cell carcinoma of the lung

A

sheets of keratin containing malignant cells

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136
Q

pathology of adenocarcinoma of the lung

A

glandular differentiation with atypia

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137
Q

features of Mycobacterium avium complex?

A

non caseating and caseating granulomas (generally in severly immunocompromised), has lung cavitations

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138
Q

pathology in TB?

A

caseating granuloma with acid fast bacilli

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139
Q

features of asthma

A

intermittent respiratory symptoms, normal CXR, sputum eosinophils, reduced FEV1<80%

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140
Q

common triggers of asthma?

A

animal dander, dust mites, pollens. cockroaches, environmental pollutants, NSAIDS, aspirin, non selective Beta blockers, URI, GERD.
Food is mostly not a trigger

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141
Q

What to suspect when a patient with MI develops acute SOB?

A

acute pulmonary oedema affecting MI of lateral ventricle. Elevated hydrostatic pressure in the pulmonary venous system leads to engorged pulmonary capillaries with transudation of fluid into the alveoli appearing as acellular pink material

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142
Q

pathology in fat embolism syndrome?

A

fat globules and bone marrow cells in pulmonary arterioles.

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143
Q

pathology in pulm h`age like Goodpasteur or other vasculitis?

A

focal necrosis of alveolar wall with intraalveolar h`age

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144
Q

pathology in chronic lung congestion?

A

hemosiderin laden macrophages (heart failure cells) as macrophages engulf the RBCs that leak from the alveolar capillaries damaged by high intravascular pressure.

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145
Q

where are elastases (neutral protease) derived from in the alveolar fluid?

A

alveolar macrophages and infiltrating neutrophils.

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146
Q

what is neutrophil elastase and macrophage elastase inhibited by?

A

serum alpha 1 trypsin and tissue inhibitors of metalloproteinases respectively.

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147
Q

what causes centriacinar and panacinar emphysema?

A

excess protease activity

148
Q

where are club (clara cells found)

A

they are no cialiated cells found in terminal portions of the bronchioles.

149
Q

what do club cells secrete

A

club cell secretory protein which protects against airway inflammation and oxidative stress and surfactant components which prevent bronchiolar collapse.

150
Q

where are goblet cells present?

A

they are present in the epithelial lining of trachea and bronchi and bronchi but not present in the more distal airways.

151
Q

what are type 1 and 2 pneumatocytes?

A

constitute over 95% of surface area of alveoli. These end differentiated squamous cells are not a major source of alveolar secretory products.
TYPE 2 are the major components of surfactant

152
Q

pulmonary chances in high altitude?

A

hypoxic pulmonary vasoconstriction (increases pulmonary vasoconstriction), increase sympathetic activity to increase cardiac output, aldosterone secretion to decrease plasma volume. Increased minute ventilation increase PaO2 and decreased PaCO2.

153
Q

renal changes in high altitude?

A

increased erythropoeitin production, increased bicarb excretion, aldosterone suppresion with diuresis and decreased plasma volume.

154
Q

blood changes in high altitude?

A

increase 2,3 DPG so increase oxygen uploading in tissues, upregulation of HIF which causes erythropoeisis and angiogenesis. Increased hb concentration and hence increased oxygen carrying capacity.

155
Q

cardiac changes in high altitude

A

increased heart rate and slightly increased cardiac output.

156
Q

brain changes in high altitude?

A

vasodilation with increased cerebral blood flow.

157
Q

histology in asbestosis

A

pleural plaques, b/l interstitial fibrosis, ferruginous bodies (golden brown or rod shaped fusiform fibers coated with iron protein complexes) has a translucent fiber core.

158
Q

features of silicosis?

A

birefreengent silicate particles, innumerable nodules that predominate in upper lung, egg shaped calcifications in hilar lymph nodes. Pleural plaques not seen.

159
Q

features in coal workers pneumoconiosis

A

carbon laden macrophages, black coal nodules distributed throughout the lungs.

160
Q

what are the physiologic changes that occur during exercise?

A

increased minute ventilation via both increased respiratory rate and increase minute volume, reduced physiologic dead space, increased V/P ratio, increase extraction of oxygen by skeletal muscle resulting in decreased mixed venous oxygen content.

161
Q

dyspnea and b/l patchy alveolar infiltrates at high altitude?

A

High altitude pulmonary oedema (HAPE)

162
Q

pathophysiology of high altitude pulmonary oedema?

A

reduced partial pressure of oxygen which leads to hypoxic pulmonary vasoconstriction and increased pulmonary arterial pressure. This leads to alveolar-capillary membrane disruption and hence pulmonary oedema.

163
Q

Clinical features of HAPE?

A

progressive dyspnea, cough, features of acute mountain sickness (headache, nausea). The hypoxemia improves with supplemental oxygen which differentiates HAPE from other causes of pulmonary oedema.

164
Q

how much is the intraplural pressure at resting equilibrium?

A

-5 cm H2O

165
Q

where is trazadone used?

A

insomnia with depression or antidepressants

166
Q

Priapism is a side effect of which drug?

A

Trazadone

167
Q

properties of trazadone?

A

serotonin modulator, has minimal effects on norepinephrine and dopamine. It is an alpha adrenergric blockage that causes hypotension and priapism. It is a histamine antagonist that causes sedation.

168
Q

What when used in conjunction with SSRI reduces the sexual side effects?

A

Buproprion.

169
Q

Which SSRis are associated with highest risk of sexual side effects?

A

citalopram and paroxetine?

170
Q

When is Phenelzine used?

A

monoamine used in resistant depression.

171
Q

What are the risk factors for ectopic pregnancy?

A

prior ectopic, pelvic surgery, PID, tobacco, IVF

172
Q

which is the most common site of ectopic pregnancy?

A

fallopian tube ampulla.

Mostly due to tubal scarring that causes embryo to implant in fallopian tube instead of uterus.

173
Q

what causes ovarian torsion?

A

rotation of ovary around infundibulopelvic (suspensory) and uteroovarian ligaments.

174
Q

clinical features of ovarian torsion?

A

sudden onset pelvic pain, nausea vomitting, adnexal mass. Doppler shows absent flow in ovaries. Rx is detorsion.

175
Q

risk factors for ovarian torsion?

A

pregnancy, ovarian induction (fertility treatment) and ovarian mass >5 cm

176
Q

clinical features of endometriosis?

A

chronic pelvic pain, dysmenorrhea, dyspareunia and infertility

177
Q

clinical features of hereditary hemachromatosis in skin?

A

hyperpigmentation

178
Q

clinical features of hereditary hemachromatosis in MSK?

A

arthritis and chondrocalcinosis

179
Q

clinical features of hereditary hemachromatosis in GI?

A

elevated liver enzymes, hepatomegaly, cirrhosis and hepatocellular carcinoma

180
Q

clinical features of hereditary hemachromatosis in endocrine?

A

DM, hypopitutarism(secondary hypogonasim due to iron deposition in pitutary gland, hypothyroidim.

181
Q

cardiac features in hereditary hemachromatosis?

A

restrictive or dilated cardiomyopathy, conduction abnormalities,

182
Q

what leads to bicornuate uterus?(indentation in the center of the fundus?)

A

failure of lateral fusion of paramesonephric ducts.

183
Q

what leads to uterine didelphys?

A

complete lack of fusion

184
Q

what is seen in hysterosalpingogram in bicornuate uterus and longitudinal uterine septum? Also what can differentiate the two?

A

on both on hysterosalpingogram there are two unfused uterine horns with central filling defect. Both can be distinguished by MRI when spetate uterus has a normal contour.

185
Q

what is mayer rokitansky syndrome?

A

complete agenesis of paramesonephric ducts

186
Q

what do mesonephric ducts form in females and males?

A

females-Gartners ducts. Males-epididymis, ductus differens, seminal vescicles and ejaculatory ducts.

187
Q

what leads to transverse vaginal septum?

A

failed vertical fusion of paramesonephric ducts

188
Q

features of peau d`orange rash?

A

generalised erythematous rash that may be tender or itchy. Skin is firm and coarsely pitted. Breast oedema. Inflammatory breast cancer. Skin changes due to lymphatic obstruction.

189
Q

which are the non invasive breast cancers?

A

DCIS and pagets

190
Q

features of DCIS

A

central necrosis, precancerous lesion, confined to ducts and lobules.

191
Q

features of Pagets

A

eczematous nipple lesion, extension of DCIS into ducts

192
Q

which are the invasive breast cancers?

A

ductal carcinoma, lobular carcinoma, inflammatory breast cancer

193
Q

features of ductal carcinoma?

A

most common type. Nests and cords of cells.

194
Q

features of lobular carcinoma?

A

small cells in single file, mammary stroma invasion.

195
Q

features of inflammtory breast cancer?

A

peau d`orange, dermal lymphatic invasion.

196
Q

features of ruptured breast implants skin changes?

A

local inflammation, granuloma and tender mass.

197
Q

features of mastitis?

A

most common in lactating women. Pain, breast swelling, erythema. fever malaise leucocytosis may be seen

198
Q

features of hypertrophic scars?

A

thick raised and pink firbous tissue line that follows the original incision

199
Q

features of keloid scars?

A

occur due to disorganised collagen deposists. Thick, rubbery and extend outside the incision borders.

200
Q

risk factors for uterine sarcoma?

A

tamoxifen use, pelvic radiation, post menopausal status

201
Q

clinical features of uterine sarcoma?

A

abnormal post menopausal bleeding, bulk symptoms like bloating and pelvic pressure, uterine mass.

202
Q

histopathology of uterine sarcoma?

A

Arises from uterine smooth muscles or endometrial stromal cells. Malignant features-cellular atypia, abundant mitosis, tumor cell necrosis.

203
Q

histopath features of uterine leiomyoma (fibroids)?

A

benign tumors of uterine myometrium caused by monoclonal proliferation of myocytes and fibroblasts.

204
Q

histopath of adenomyosis?

A

endometrial glands embedded in the myometrium

205
Q

histopath of chronic endometritis?

A

plasma cells within the endometrial stroma

206
Q

features of genital herpes?

A

casused by HSV 2 . Tender inguinal lymphadenopathy, vesicles.

207
Q

most common sequelae of HSV 2

A

recurrent genital lesions sas HSV remains dormant in the sarcal root ganglia.

208
Q

causes of erectile dysfunction?

A

organiclike hypogonadism, neuro, arterial (aortoiliac occlusion pain in buttocks, post thigh and calves during exercise) or it can be phychogenic

209
Q

risk factors of psychogenic erectile dysfunction?

A

marital stress, psychosocial trauma, severe medical illness (MI, stroke), mood and anxiety disorders.

210
Q

features of psychogenic erectile dysfunction?

A

abrupt onset, clear precipitationg stressor. Situational ED (normal nocturnal erections), impaired or premature organsm.
managed by cognitive/behaviour therapy. Couples/relation therapy.

211
Q

how are erections affected in BPH?

A

semen vol reduced in BPH. BPH surgery causes retrograde semen into bladder. Erectile dysfunction if taking finesteride.

212
Q

how does testosterone deficiency affects erections?

A

loss of libido and loss of normal nocturnal erections.

213
Q

what is the cause of post menopausal bleeding in an obese woman?

A

peripheral aromatisation of androgens (by aromatase enzyme in adipose tissue) to estrogen in the adipose tissue leads to chronic unopposed estrogen exposure and uncontrolled endometrial proliferation.

214
Q

featutres of hyperprolactenemia?

A

headaches, bitemporal hemianopsia from mass effect, decreased GnRH hence decreased FSH and LH amenorrhea

215
Q

Is endometriosis common after menipause?

A

No. Endometriosis is very uncommon after menopause as it requires very high level of premenapausal estrogen that is not even found in obese post menopausal women.

216
Q

Histology of mature benign teratoma?

A

multiple germ layers (endoderm, ectoderm, mesoderm). Cystic may contain sebaceous content, hair and teeth. Hair follicles, sebaceous glands, bone, respiratory epithelium, and thyroid tissue found.

217
Q

histology in high grade serous ovarian carcinoma

A

ovarian stromal invasion by atypical cells forming papillae and glandular spaces.

218
Q

histology in PCOD?

A

cystic follicles and stromal fibrosis . Generally many masses not a single mass.

219
Q

feautures of high grade CIN cervical intraepithelial neoplasia?

A

atypical squamous cells have invaded beyond the lower one third of the cervical epithelium.
In low grade CIN they have not invaded past
Basement membrane invasion signifies carcinoma

220
Q

histopath in HPV infection?

A

perinuclear vacuolisation (koilocytic change) due to viral proteins.

221
Q

major risk factor for acute simple cystitis in girls?

A

it is caused by ascending infection when enteric flora ascend from the urethra to the bladder. Major RF is sexual intercourse

222
Q

what is the mode by which pyelonephritis is caused?

A

hematologic infection that enters through the glomeruli to reach urinary tract. Patients generally sick with fever and chills.

223
Q

features of subserosal uterine leomyoma

A

irregular uterine enlargement, poat ones cause pelvic pressure, constipation. Anterior ones cause urgency, incomplete emptying.

224
Q

how is uterus enlarged in adenomyosis?

A

uniformly enlarged.

225
Q

features of rectovaginal endometriosis?

A

pelvic pain and constipation around menses. Dyapanernuria, dyschezia and tender nodularity present.

226
Q

where does fluid accumilate in communicating hydrocephalus?

A

in tunica vaginalis in the setting of patent processus vaginalis.

227
Q

what is Peyronie disease?

A

excess collagen formation within tunica albugenia that can cause significant pain and curvature of the penis.

228
Q

Describe the 3 spermatic fascia?

A

Internal spermatic fascia immediately overlies the spermatic cord and is derived from transversis vaginalis.
Cremasteric fascia arises from the internal oblique abdominal muscle.
External spermatic fascia arises from external oblique abdominal muscle.

229
Q

what are the physiologic factors for insulin induced weight gain?

A

increased peripheral glucose uptake, increased adipose fatty acid uptake, reduced renal glucose losses

230
Q

what behavioural factors can cause insulin induced weight gain?

A

less rigorous dietary adherance, eating/snacking in response to hypoglycemia.
counselling should include patients perspective on appetite, changes in dietary patterns and hypoglycemic episodes.

231
Q

what is the cause of primary congenital hypothyroidism?

A

abnormal thyroid development like agenesis, hypoplasia or ectopic location like lingual, mediastinal.

232
Q

clinical features of congenital hypothyroidism

A

asymptomatic at birth as maternal T4 crosses the placenta. After few weeks to months lethargy, poor feeding, enlarged frontanelle, protuding tongue, puffy face, umbilical hernia, constipation, prolonged jaundice, dry skin.

233
Q

what causes neonatal graves disease?

A

transplacental transfer of maternal thyroid stimulating antibodies

234
Q

why do patients with long standing DM 1 have high risk of hypoglycemia?

A

insulin will be continued to be absorbed from the injection site and also there is decreased glucagon secretion from alpha cell failure.

235
Q

what are the physiologic changes that occur with hypoglycemia?

A

insulin secretion by pancreatic beta cells decreases leading to decreased peripheral uptake and utilisation of glucose. Alpha cells increase secretion of glucagon which is the counter regulatory hormone to insulin and acts on liver to rapidly increase glycogenolysis and gluconeogenesis and decrease glycolysis. There is increase in epinephrine that causes increase hepatic glucose production. It can also increase cortisol and growth hormone that increases glucose.

236
Q

what happens when there is downregulation of insulin receptors due to prolonged exposure to insulin?

A

hyPERglycemia

237
Q

what causes hypoglycemia during exercise?

A

muscle contraction and insulin increase GLUT4 translocation to the cell surface and hence decreases blood glucose level.

238
Q

where is GLUT 2 found?

A

liver and pancreatic beta cells.

239
Q

Thyroid hormones in congenital hypothyroidism and transient due maternal exposure?

A

decreased free and total T4 and increased TSH

240
Q

thyroid hormones in central hypothyroidism?

A

decreased free and total t4 and TSH

241
Q

resistance to thyroid hormones?

A

elevated T4 and TSH. Insensitivity to T4

242
Q

thyroid gland resistance to TSH

A

same like primary hypothyroidism but thyroid gland normal.

243
Q

causes of primary hyperalstosteronism?

A

unilateral adrenal adenoma (Conn) and bilateral adrenal hyperplasia, both can be differentiated on CT

244
Q

features of hyperaldosteronism

A

hypernatremia, hypokalemia, met alkalosis

245
Q

features of primary adrenal insufficiency

A

hyponatremia, hypovolumia, hyperkalemia, met acidosis

246
Q

what antibodies are found in Graves?

A

thyroid receptor antibody

247
Q

what are the two clinical features specific to Graves disease?

A

thyroid dermopathy and graves opthalmopathy as these are caused by autoimmune responses directed towards the TSH receptors that results in accumalation of glycosaminoglycans within the affected tissues.

248
Q

which are the highest risk factors for coronary artery disease?

A

noncoronary atherosclerotic disease, diabetes mellitus, chronic kidney disease.

249
Q

what is the major risk factor for ESRD?

A

DM, followed by HT.

50% of patients with ESRD die of cardiovascular disease.

250
Q

common etiologies of gynacomastia in males?

A

increased estrogen levels (cirrhosis, obesity), decreased testosterone levels (CKD, hypogonadism), meds decreased androgen production(GnRH agonists, ketoconazole), decreased conversion to DHT (5 alpha reductase inhibitors), inhibition of androgen receptors (spirinolactone, bicalutamide).

251
Q

why do people with prostate cancer get gynacomastia? how is it treated?

A

due to androgen deprivtaion therapy, treated with Tamoxifen.

252
Q

which of the cholesterol lowering drugs cause hypertriglyceredemia?

A

bile acid binding resins

253
Q

which the is the first line treatment for hypertriglyceredemia?

A

fibrates

254
Q

patient who failed first line therapy of BPH (must have then been prescribed 5 alpha reductase inhibitors like finesteride) how does it lead to gynacomastia?

A

increase peripheral conversion to testosterone to estrogen.

255
Q

what will levels of ACTH, CRH and cortisol be in pitutary tumor or infacrtion?

A

ACTH and cortisol low and CRH high

256
Q

how does thiozolididiones decrease blood glucose

A

decreasing insulin resistance (circulating levels of insulin will decrease over time) Act like activating PPAR.

257
Q

what is the etiology of DM-1

A

autoimmune destruction of pancreatic beta cells causing insulin deficiency.

258
Q

clinical features of DM-1

A

polyuria, polydypsia, weight loss, polyphagia, blurred vision, ketoacidosis

259
Q

diagnosis of DM-1?

A

fasting glucose >126, Hb A1c>6.5, random glucose >200, oral glucose tolerance test

260
Q

Addition of what in the blood of the patient with hemophilia will cause clotting?

A

Thrombin.
Thrombin mediates cleavage of fibrinogen to form fibrin, hence without thrombin, fibrinogen alone will not help form a clot.

261
Q

function of protein C?

A

physiologic anticoagulant that degrades factor 5 a and 8 a

262
Q

function of urokinase?

A

concerts plasminogen to plasmin which breaks down fibrinogen and fibrin into their degradation product and hence helps in breaking a clot.

263
Q

pathyphysiology in hemachromatosis?

A

HPE normally interacts with transferrin receptors to sensor iron stores. In hemachromatosis there is a mutation in HPE that detects falsely low iron stores and hence there is iron accumalation. Enterocytes increase DMT1 and hepatocytes decrease hepcidin.

264
Q

where is basal ganglia atrophy seen?

A

wilson disease

265
Q

anemia with decreased MCV?

A

iron def, thalesemia, lead intoxication, sideroblastic

266
Q

anemia with increased MCV?

A

folate and B12 deficiency

267
Q

anemia with normal MCV and decreased reticulocyte count?

A

leukemia, aplastic anemia, anemia of chronic disease

268
Q

anemia with normal MCV and increased retic count?

A

H1age, hemolysis (g6pd, spehrocytosis, autoimmune, microangiopathic)

269
Q

features of iron def anemia?

A

low iron, low iron saturation, low retic, increased TIBC and increased gtransferrin, microcytic and hypochromic RBC

270
Q

where is hypersegmented neutrophils seen?

A

B12 and folate deficiency

271
Q

most common deficiency in vegetarians?

A

folate is more common as b12 deficiency takes several years to build up.

272
Q

Patient with echymosis, epistaxis and isolated thrombocytopenia what should be most likely diagnosis?

A

ITP in which there are autoantibodies to platelets, large plts seen on smear. Treatment is immunosuppression.

273
Q

What are the causes of aplastic anemia (in which there is pancytopenia?)

A

parvovirus, EBV, high dose chemotherapy, radiation

274
Q

what are features of vWD?

A

NORMAL plt count, prolonged bleeding time and PTT

275
Q

features of CO poisoning?

A

increases carboxyhemoglobin content, but no effect on PaO2 and does not precipitate methmemoglobinemia.
Shifs o2 dissociation curve to left

276
Q

how does cdk4/6 inhibitors work?

A

CDK4/6 control progression of cell growth from G1–>S by clyclin D.
CDK 4/6 inhibitors stop cellular replication in rapidly dividing hematopoeitic cells particularly kin bone marrow and hence can cause myelosuppresion.

277
Q

What is the side effects of immunotherapy that targets PD1, PDL1, CTLA4?

A

autoimmune related adverse events including skin, liver, GI and endocrine inflammation

278
Q

cardiomyopathy is a side effect of which chemotherapy?

A

anthracyclines(doxorubicin) and HER2 antibodies *trastuzumab)

279
Q

sensorineural hearing loss is the side effect of which chemotherapy?

A

cisplatin

280
Q

peripheral neuropathy is the side effect of which chemotherapy?

A

bortezomib

281
Q

which chromosomal translocation and cytogenetics is seen in AMPL?

A

PML/RARA , t(15,17)

282
Q

which translocation is seen in Burkitts?

A

t(8, 14)

283
Q

which translocation is seen in mantle cell lymphoma?

A

t(11,14)

284
Q

what cytogenetics seen in CLL?

A

deletion of 13q

285
Q

features of polycythemia vera?

A

increased RBC mass, increased plasma volume, low erythropoeitin levels. There is JAK2 mutation rendering hematopoeitic stem cells more sensitive to growth factors.

286
Q

histopath of spleen in sickle clel disease?

A

atrophy and fibrosis due to repeated infarctions

287
Q

when is white pulp hyperplasia seen in spleen?

A

infection or malignancy

288
Q

features of follicular lymphoma?

A

most common indolent NHL, waxing and waning course, presents in middle aged with painless lymphadenopathy, abdominal mass. t(14,18) translocation seen.
Histology shows a mixture of cleaved and non cleaved follicular center cells.

289
Q

what is hairy cell leukemia positive for?

A

TRAP. Presents with pancytopenia and splenomegaly in older men.

290
Q

how does diffuse large B cell present?

A

rapidly enlarging nodal (mediastinal, neck, abdomen) or extranodal symptomatic mass

291
Q

common sites of Burkitt?

A

it is the most rapidly dividing, seen in facial bone, jaw, abdomen

292
Q

what is mycosis fungoides?

A

cutaneous T cell lymphoma

293
Q

mechanism of iron def in anemia of inflammation as seen in RA?

A

increased hepcidin which increases sequestration of iron within the reticuloendothelial system and decreases circulating iron. There is increase in bone marrow iron levels. Decreased serum iron, iron binding capacity and decreased retic.

294
Q

what kind of hemolysis seen in SLE, CLL?

A

extravascular hemolysis, igG autoantibodies formed against RBC membrane which are identified by Fc receptor on splenic macrophages

295
Q

what kind of hemolysis is seen in mycoplasma?

A

Intravascular, IgM involved

296
Q

features of microangiopatic hemolytic anemia?

A

caused by shearing of RBcs in the microvasculature
due to formation of fibrin rich platelet clots.
Normocytic anemia, reticulocytosis and severe thrombocytopenia (around 10,000)

297
Q

What is seen in peripheral smear in hemolytic anemia?

A

polychromasia, spherocytes, nucleated RBCs

298
Q

what cells are seen in thrombotic microangiopathy?

A

schistocytes

299
Q

where are hypersegmented neutrophils seen?

A

B12 deficiency

300
Q

how does inflammation cause thrombocytosis?

A

IL6 causes liver to produce thrombopoeitin which causes megakaryocyte proliferation and maturation. This is reactive thrombocytosis.

301
Q

what is essential thrombocythemia

A

myeloproliferative disorder with autonomous clonal proliferation of megakaryocytes, vasomotor symptoms(dizziness) and risk of thrombosis.

302
Q

feature of myelofibrosis?

A

extramedullary hematopoeisis (hepatosplenomegaly)

303
Q

why do older patients with traumatic blood loss have lower retic and longer recovery time?

A

due to decreased bone marrow mass and increased bone marrow fat leading to impaired marrow reserve.

304
Q

Moa of warfarin and reversal?

A

decreased production of vitamin K dependant factors. Reversal PCC (prothrombin complex concentrate, IV Vit K)

305
Q

MOA of dabigatran and reversal?

A

direct inhibition of clot bound and free thrombin. Reversal Idarucizumab (mab fragment that binds dabigatran), PCC

306
Q

MOA and reversal of rivaroxiban and apixiban?

A

direct inhibition of factor Xa. Reversal recombinant modified factor Xa (andexanet), PCC

307
Q

MoA and reversal of heparin?

A

increased activity of ATIII. Reversal protamine.

308
Q

changes in athlete heart to left ventricular ejection fraction, left ventricular cabity size, maximum cardiac output?

A

unchanged, increased, increased

309
Q

is mitochrondrial DNA maternally derived? Examples of mitochrondrial disease

A

Yes

Leigh and MELAS

310
Q

cleft lip is failure of fusion of what?

A

maxillary prominence and intermaxillary segment

311
Q

holoprosencephaly is failure of fusion of what?

A

failure of nasal median prominence to fuse and form intermaxillary segment

312
Q

cleft palate is failure of fusion of?

A

palatine shelves fail to fuse with one another or with the primary palate.

313
Q

which nerve is involved in temporomandibular joint disorder?

A

mandibular nerve CN V3 (of trigeminal nerve)

314
Q

what causes ear pain in TMD and ear stuffiness?

A

ear pain mandibular, ear stuffiness hypersensitivity to tensor tympani

315
Q

feature of erythema migrans?

A

lyme, target lesion annukar lesion with central clearing spreads through dermis.

316
Q

how does drug induced cytotoxic fixed drug eruption look?

A

dusky plaque

317
Q

noise induced hearing loss causes damage to what ?

A

stereociliated hair cells of the organ of Corti

318
Q

which part of the ear registers low frequency sounds?

A

distal cochlea

319
Q

pathophysiologic changes in ascites?

A

decrease plasma oncotic pressure, splanic vascular resistance and effective arterial blood volume, normal capillary permeability

320
Q

pathophysiologic changes in congestive heart failure?

A

low EABV, increased splanic resistance. Oncotic pressure and capillary permeability are unaffected.

321
Q

pathophysiologic changes in nephrotic syndrome?

A

increase capillary permeability, decreased oncotic pressure, increased EABV, splanic resistance is unaffected.

322
Q

which nerve is in close proximity to inferior thyroid artery?

A

recurrent laryngeal nerve

323
Q

symptoms of unilateral and bilateral paralysis of recurrent laryngeal nerve?

A

unilateral-hoarseness, bilateral-respiratory distress and inspiratory stridor due to complete vocal cord paralysis.

324
Q

where is ciliated pseudostratified columnar epithelium seen in respiratory tract and function?

A

nasal cavity, upper pharynx, false vocal cords, trachea, bronchi… function-mucus secreting cells mositen air and trap debris and pathogens

325
Q

where is startified squamous epithelium seen in respi? function?

A

true vocal cords,, function-protects from abrasion and chemical attack

326
Q

where is cuboidal epithelium seen in respi?function?

A

bronchioles,, function- conduct air to alveoli

327
Q

where is simple squamous epithelium seen in respi tract? function?

A

alveoli,, function- gas exchage

328
Q

why does HPV affect true vocal cords?

A

it has prelicdiction for stratified squamous epi like vaginal, anal canal, cervix, true vocal cords
Infants acquire respiratory papillarilomatosis through birth canal of infected mothers and present with hoarseness, weak cry and stridor

329
Q

how does inactivated vaccine provide immunity?

A

humoral immunity. preventing viral entry into the cells

330
Q

how does live vaccine provide immunity?

A

strong cell mediated immune response that can kill virally infected cells

331
Q

how does inactivated influenza virus give immunity?

A

by forming antibodies against the hemagglutinin of induced strains thus preventing the hemagglutinin to bind to sialic receptor of host respi epithelium cells

332
Q

what do different colors mean in melanoma?

A

red-vessel ectasia dilatation and inflammation, brown or black-neoplastic melanocytes, white-occurs when cytotoxic T cells recognise tumor antigens and induce apoptosis leading to malignant melanocyte regression.
Melanocyte regression is a hallmark of treatment with PD-1 inhibitor

333
Q

what granules do reactive lymphocytes have?

A

cytotoxic granules composed of perforin and granzymes

334
Q

which cells secrete elastase?

A

neutrophils and macrophages

335
Q

what is responsible for IL2 anticancer effect in melanoma and renal cell carcinoma?

A

increased T cell and NK cells

336
Q

MOA of Bevacizumab?

A

interfers with VEGF receptor activation thereby inhibiting angiogenesis

337
Q

MOA of Alemtuzumab?

A

anti CD 52, used in CLL. initiates direct cytoxic effect through complement fixation and antibody dependant cell mediated toxicity

338
Q

what is Adalimumab and uses?

A

recombinant human IgG that binds to TNF alpha

339
Q

what can cause worsening symptoms for someone on Adalimumab?

A

anti drug antibodies can form which block its interaction with TNF alpha which reduces activity and causes rapid drug clearance

340
Q

what process is useful in eliminating T cells that bind to self MHC or self antigens? Where does this occur?

A

Negative selection

Occurs in thymic medulla

341
Q

Pathophysiology of ankylosing spondylitis?

A

Increased IL17, TNFalpha

Increased risk with HLA B 27

342
Q

CF of ank spondylitis?

A

Insidious onset of back and buttock pain (onset before 40 yrs, relived by exercise and not rest, nocturnal pain), reduced chest expansion and spinal mobility, enthesitis, dactylitis, ant uveitis

343
Q

Lab/imaging in ankylosing spondylitis?

A

elevated ESR and CRP, sacroilitis, bridging syndesmophytes(bamboo spine)

344
Q

treatment of ank spondylitis?

A

NSAIDS, anti TNFalpha like infliximab and etanercept, andti IL17 like secukinumab

345
Q

function of IL 2 and interferon gamma?

A

activation of response for viruses and mycobacterium

inhibitis Th17 cell differentiation

346
Q

function of IL4?

A

differentiation of naive Th cells into Th2 subsets, alternate macrophage activation (M2 type) and IgE production

347
Q

function of IL5?

A

B cell growth, IgA production and eisinophils

348
Q

what weight is used for dosing in obese patients in case of hydrophilic drugs?

A

lean body weight or adjusted body weight

as distribution of drug is limited to ECF

349
Q

difference between NMS and serotonin syndrome?

A

NMS has diffuse (lead pipe rigidity and hyporeflexia).

Serotonin syndrome has clonus and hyperreflexia

350
Q

Difference between first and zero order kinetics (this q had a lot of graph explanation with points)

A

In first order a constant fraction of drug is metabolised per unit time so the amount metabolised changes based on the serum concentration. In zero order kinetics a constant amount of drug is metabolised per unit time independent of serum levels.

351
Q

what causes impaired drug clearance in cardiac failure?

A

impaired perfusion to excreting organs like liver, kidneys.

352
Q

which enzyme deficiency is seen in Gauchers?

A

lysosomal beta glucocerebrosidase

353
Q

symptoms of Gauchers?

A

hepatosplenomegaly, pancytopenia and bone pain. Lipid laden macrophages (wrinkled tissue paper appearance).

354
Q

Treatment of gauchers? Route?Entry into cells?

A

recombinant glucocerebrosidase given IV, entry by binding to mannose 6 phosphate on the cells and inducing apoptosis

355
Q

symptoms of cyanide poisoning?

A

altered mental status,seizures, cvs collapse, bright red venous gas (seen of venous gas and funduscopy)

356
Q

3 drugs used in cyanide poisoning and MOA?

A

sodium nitrite- promotes methhb formation which combines with cyanide to form cyanmethhb.
Sodium thiosulfate- serves as sulfur donor to promote hepatic rhodonese-mediated conversion of cyanide to thiocyanate which is excreted in urine.
Hydroxocobalamin- cobalt moiety binds to intracellular cyanide ions and forms cyanocobalamin which is excreted in the urine

357
Q

meds that cause hypotension and bradycardia? and distinguishing features of each?

A

beta blockers- hypoglycemia, bronchospasm, heart block
CCB- hyperglycemia
Digoxin– hyperkalemia, scooped ST segments on ECG
Clonidine- miosis, respi suppression
cholinergics- SLUD
Magnesium- Hyporeflexia

358
Q

why should you wait atleast 2 weeks after MOA inhibitor like phenelzine is stopped and to restart new SSRI?

A

these two weeks helps to regenrate monoamine oxidase othweise coadministration of both can cause serotonin syndrome

359
Q

symtpoms of serotonin syndrome?

A

AMS, neuromuscular excitation (hyperreflexia, clonus), and autonomic hyperactivity (hypertthermia, tachycardia, diaphoresis)

360
Q

how does lithium exert its antimaniac and antidepressant effect?

A

inositol monophosphate inhibition

361
Q

what improves CNS penetration of drugs?

A

inhibition of p glycoprotein which is an efflux pump on the brain capillary endothelial cell

362
Q

what are the features of drugs that are excreted through the liver?

A

high lipid solubility and high volume of distribution

363
Q

Indications and SE of mood stabilizers in bipolar disorders?

A

lithium: used in maniac and depressive features, SE are DI, hypothyroidism, tremor, EBstein anomaly
Valproate: used in manic, SE are hepatotoxicity, neural tube defects
Carbamazepine: used in maniac, SE are aplastic anemia, SIADH, neural tube defects
Lamotrigine: used in depressive features. SE are Steven johnson

364
Q

SE of citalopram? clonazepam? resperidone?Trazadone?

A

sexual dysfunction
agranulocytosis
weight gain, hyperprolactenemia (galactorrhea, amenorrhea)
priapism

365
Q

drug metalobised by acetylation?

A

isoniazid

Follows bimodal distribution with slow and fast acetylators

366
Q

drugs metabolised by methylation?

A

azathioprine and 6 MP

367
Q

why are some drugs less effective in newborns compared to adults?

A

higher proportion of total body water results in lower plasma concentration of water soluble drugs

Uworld (2 decks)

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