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STEP 1 MIXED > Deck 10 > Flashcards

Deck 10 Flashcards

1
Q

Difference between OR and RR?

A

OR is done in a case-control study. Cases are asked about previous exposure** to the risk factor.

RR is done in prospective/retrospective cohort studies followed over time and then assessed for development of the disease

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2
Q

Equation OR?

A

OR = Odds of exposure in cases/ odds of exposure in controls

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3
Q

What is a case-control study?

A

You find people who have the disease and compare them to people who don’t have the disease. Ask about previous risk factors (ie. smoking or NSAID use)

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4
Q

What is the genetic and cellular cause for polycythemia vera?

A

Janus kinase 2 (JAK2) mutation

Overactive cytoplasmic non-receptor tyrosine kinase

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5
Q

Who gets acalculous cholecystitis?

A

Critically ill patients. Due to stasis and ischemia of gallbladder. Won’t see any stones but will still have other signs of cholecystitis

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6
Q

What will SIADH present with clinically?

A

Symptoms of hyponatremia, euvolemic hyponatremia***, low serum osmolality.
No features of volume overload
Small cell lung carcinoma

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7
Q

Where do the gastric fundus veins drain to? Why is this clinically significant?

A

Into splenic vein
If there is Splenic thrombosis (due to pancreatic inflammation) then these veins can become engorged and cause gastric varices + bleeding

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8
Q

What are serum markers for rheumatoid arthritis?

A

Anti-CCP and RF

IgM against Fc portion of IgG

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9
Q

What does it mean if PaO2 and SaO2 are normal, but there is decreased oxygen content?

A

Anemia. Chronic blood loss

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10
Q

What drug inactivates 6-MP?

A

Xanthine oxidase. Creates inactive metabolites

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11
Q

WHat does it mean if secretin paradoxically stimulates the release of gastrin?

A

Gastrinoma, Zollinger-ellison syndrome

secretin normally inhibits release of gastrin from G cells

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12
Q

What does high urine Cl- in metabolic alkalosis mean?

A

Mineralcorticoid excess (saline unresponsive)

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13
Q

What do alpha and beta cells in pancreas secrete?

A

alpha - glucagon

beta - insulin

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14
Q

Which cells increase bicarb secretion?

A

Duodenal S cells release secretin, which stimulates exocrine pancreas to secrete bicarb rich, chloride poor fluid

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15
Q

WHat is the middle meningial artery a branch of?

A

Maxillary artery

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16
Q

What does multiple myeloma do to bone remodelling cells?

A 
Increases osteoclast (activates RANK)
Inhibits osteoblasts (destroys OPG)
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17
Q

What does estrogen do to cell communication during labor?

A

Increases gap junctions (connexins) to increase myometrial excitability

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18
Q

Clinical symptoms NF-1? Inheritance?

A

AD. Chrom 17

Cafe au lait spots, neurofibromas, lisch nodules, brain tumors, bony abnormalities

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19
Q

MOA for fibrates and fish oil lowering cholesterol?

A

Decrease hepatic VLDL receptor production via activating PPAR-alpha

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20
Q

What class of antibiotic is cefuroxime?

A

2nd gen cephalosporin

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21
Q

Clinical features of NMS?

A

Muscle rigidity, hyperthermia, confusion, autonomic instability

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22
Q

What is tx for NMS, including muscle rigidity?

A

Discontinue antipsychotics + dantrolene (inhibition of calcium ion release from SR) - muscle relaxant

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23
Q

SE of glyburide?

A

Sulfonylurea- risk of hypoglycemia

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24
Q

MOA sulfonylureas?

A

Inhibits K+ efflux from pancreatic beta cells, causes depolarization and release of insulin

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25
Q

Which class I antiarrhythmics increase length of action potential?

A

Class IA - quinidine, procainamide, disopyramide

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26
Q

Which class I antiarrythmics shorten length of AP?

A

Class IB Lidocaine, mexiletine

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27
Q

Which class I antiarrhythmics have no affect on length of AP?

A

Class IC Flecainide, propafenone

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28
Q

What causes degeneration of posterior columns and lateral coritcospinal tract?

A

B12 deficiency
Numbness, parasthesias, loss of proprioception
**upper motor neuron signs due to degeneration of lateral corticospinal tracts

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29
Q

Where are areas of demylination in tabes dorsalis?

A

Dorsal columns and dorsal roots. Impaired position, vibration, sensation, ataxia, and pain, parasthesias

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30
Q

Kidney- subendothelial deposits with PAS pink stain. What is it?

A

Diabetic nephropathy– hyaline arteriolosclerosis

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31
Q

WHat is limit for $$ you are allowed to accept as gifts from patients?

A

$10

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32
Q

What does protein C do?

A

It acts as antithrombolytic by inactivating factor V

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33
Q

What is factor V Leiden?

A

Factor Va is resistant to protein C inactivation, so individual is in a prothrombotic state

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34
Q

What drug shouldn’t be given with statin?

A

Gemfibrozil (fibrates). Increase risk of statin-induced myopathy. Impair hepatic clearance of statins

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35
Q

What is heteroplasmy?

A

The same disease causes varying amount of clinical symptoms in different individuals with that disease because of genetic mixing of material. Ie. mitochondreal disease in two sibilings is much worse in one than the other because some cells got the bad mitochondrea and others got the good ones

36
Q

What causes warfarin induced necrosis?

A

Warfarin inhibits protein C and S, which induces a hypercoagulable state

37
Q

In a hypoglycemic state, why do you check C-peptide?

A

To determine whether the insulin is endogenous (high C-peptide) or exogenous (low C-peptide)

38
Q

How does glucose cause depolarization of pancreatic beta cells?

A

Oxidative phosphorilation after transport through GLUT-2 proteins. This generates ATP, which binds K+ channels to close them and cause depolarization and insulin release

39
Q

Child with albinism, immunodeficiency, and neurologic defects, nystagmus. Giant cytoplasmic granules in neutrophils and macrophages. What is it?

A

Chediak-Higashi syndrome

Failure of phagosome-lysosome fusion

40
Q

Man with pleural effusion, unilateral pleural thickening. Histology- long slender microvilli and abundant tonofilaments. Immunohistochemical markers show pancytokeratin. What is it?

A

Mesothelioma

41
Q

How do you treat an episode of severe hypoglycemia in medical vs nonmedical setting

A

IV dextrose in hospital

IM glucagon out of hospital

42
Q

What is equation for maintenance dose?

A

Maintenance dose = Steady state plasma concentration x CL/ bioavailability fraction

43
Q

WHat is atropine used for?

A

Anticholingergic drug given pre-surgery to decrease bronchial secretions and promote bronchodilation. Can result in anticholingergic toxicity

44
Q

What is antidote to atropine overdose?

A

PHysiostygmine (cholinestrase inhibitor)

45
Q

Symptoms of anticholinergic toxicity?

A

Dry mucous membranes, hyperthemia, flushed skin, cycloplegia, mydriasis, altered mental status, urinary retention, constipation, tachycardia

46
Q

Woman with mobiliform rash, flaccid paralysis, headache, confusion, and meningitis. What is it?

A

West nile virus

47
Q

What is transference (psych?)

A

When a person unconsiously treats a person in the present as if they were a person from their past (i.e. treating a doctor as if they were one of their parents)

48
Q

What is the effect of epinephrine on HR and BP in low doses? High doses?

A

Always: B1 > B2 > A1 agonistic effects
Will increase HR and systlic BP no matter what
HOWEVER
Diastolic low dose: B2 > A1 (lowers BP)
Diastolic high dose: A1 > B2 (Heightens BP)

49
Q

What does epinephrine + beta blockers do?

A

Will cause unopposed A1 stimulation. The Increase in diastolic BP and reflexive bradycardia

50
Q

What part of brain do SSRIs work on?

A

Raphe Nuclei

51
Q

What is Tx for carcinoid syndrome?

A

Octreotide and surgical resection

52
Q

Primary cause of normal pressure hydrocephaus?

A

Decreased CSF reabsorption

53
Q

Most likely complication of varicose veins?

A

Skin ulcerations

54
Q

What do MHC II display? MHC I?

A

MHC II display exogenous antigens - only found on APCs

MHC I display endogenous antigens (tumors, viral infections)

55
Q

What is difference in processing for MHC I and MHC II?

A

MHC II undergo acidification of lysosomes

56
Q

How does warfarin-induced necrosis occur?

A

Warfarin inhibits Protein C, which is a anticoagulant for vit K factors
Causes microvascular occulsion

57
Q

Function of RER and smooth ER?

A

RER: transfer of proteins to extracelluar space and cell membrane

SER: lipid synthesis, carbohydrate metabolism, detoxification of subtances

58
Q

What is wilson’s disease? What are clinical signs?

A

Copper overload, AR disease
Kay-fleisher rings, chronic liver failure, parkinsonism, disarthria, gait abnormalities, depression, psychiatric symptoms, personality changes
*decreased ceruloplasmin in serum, increased urinary copper excretion

59
Q

Tx wilson’s disease?

A

D-penicillamine (free sulfhydryl group and copper chelator)

60
Q

Tx iron overdose?

A

Deferoxamine

61
Q

Tx lead poisoning?

A

EDTA

62
Q

What layers do you go through to do cricothyrotomy?

A

Skin
Superficial cervical fascia (subcu fat and platysma muscle)
Investing and pretracheal layers of deep cervical fascia
Cricothyroid membrane

63
Q

What is bronciolitis obliterans? Who gets it?

A

Ingrowth of granulation tissue into small airways. Decreases FEV1 - chronic lung transplantation rejection (>6 months)

64
Q

What is the cellular cause of acute, hyperacute, and chornic lung rejection?

A

Hyperacute- Preformed host antibodies to donor ABO or HLA (min to hrs)
Acute (<6months) CEllular antibody response to HLA
Chronic (>6 months) low grade cellular response to donor HLAs

65
Q

What part of lung is affected in hyperacute, acute, and chronic lung rejection?

A

hyperacute- neutrophilic intfiltration with fibrinoid necrosis and thrombosis
Acute- small lung vessels (perivascular) and bronchiole (submucosal) lymphocytic infiltrates, alveolar walls
Chronic- small airways (bronchiole, submucosal) graulation and scarring (broniolitis obliterans)

66
Q

What are abnormal labs for the following:

Hemophelia (A&amp;B)
vWF deficiency
DIC
Heparin
Warfarin
ITP
A

Hemophilia A&B raised aPTT
vWF disease raised aPTT and bleeding time
DIC raised PTT aPTT bleeding time decreased platelets
Heparin raised aPTT
Warfarin raised PTT
ITP low platelets raised bleeding time

67
Q

Why is the Hib vaccine a polysaccharide conjugated to a carrier protein (tetanus toxoid?)

A

It not only creates B cell response, it elicits a T cell response which allows for creation of memory B cells

68
Q

Virchow’s triad?

A

Venous stasis, hypercoagulability, endothelial damage

69
Q

How are phosphate and calcitriol levels affected in CKD?

A

Hyperphosphatemia due to decreased GFR

Phosphate causes release of FGF-23 from bone, which inhibits calcitriol (1-25 dihydroxyvitD) production

70
Q

What is polygenic inheritence? Example?

A

Two or more genes will contribute to a person having the disease. Multiple people in the family have the disease, but in no discernable pattern

Androgenic allopeica

71
Q

What are genetic causes of DS?

A

Meiotic nondisjunction
Unbalanced translocations
Mosaicism

72
Q

What does raised procalcitonin level signify? Low level?

A

Raised- presence of bacterial toxins
Low- presence of viral infection

Produced by monocytes and thyroid cells

73
Q

What is the only thing that changes in diastolic heart failure with preserved EF?

A

L ventricular end diastolic pressure is increased

Volume not affected

74
Q

Tx cholesterol gallstones?

A

Bile acid supplementation (hydrophilic) - ursodeoxycholic acid

75
Q

What is the MoA for trimethoprim, methotrexate, and pyrimethamine?

A

Inhibits confersion of folate to THF by inhibiting DHFR.

76
Q

Why are TMP-SMX given together?

A

They both block production of THF. Sulfonamdes inhibit an earlier step of folic acid pathway in bacterial cells

77
Q

What nerve is at risk during appendectomy? What does it supply?

A

Iliohypogastric nerve

Supplies lateral abdominal wall muscles and cutaneous sensation to suprapubic and gluteal regions

78
Q

How does TNF-alpha inhibit glucose uptake?

A

Activates serine kinases** that phosphorylate serine residues*** and inhibits tyrosine phosphorilation. Inhibits actions of insulin

Glucocorticoids catecholamines, and glucagon all create insulin resistance in the same way

79
Q

Symptoms of lambert-eaton syndrome? What condition is it associated with?

A

Proximal myopathy, oculobulbar neuropathy, diplopia, ptosis, dysarthria, autonomic symptoms (dry mouth or impotence)

Small cell lung cancer

80
Q

Why is taz given with penicillin?

A

It acts as a beta lactamase inhibitor

81
Q

What congenital disorder results in maternal virilization?

A

Aromatase deficiency

82
Q

Where do acoustic swchwannomas normally appear?

A

Cerebellopontine angle

83
Q

Which nerves are compressed by schwannomas?

A

CN V, CN VII, CN VIII

84
Q

What do basophilic nuclei with intensely eosinophilic cytoplasm mean in brain?

A

Irreversible neuronal damage (red neurons). Will cause glial hypertrophy afterward via astrocytes

85
Q

How does amphotericin B cause nephrotoxicity?

A

Binds cell membrane cholesterol

Also responsible for hypomagnesemia and hypokalemia

86
Q

What conditions raise MCHC?

A

SS, hereditary spherocytosis

STEP 1 MIXED (13 decks)

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