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step II > amboss 7/10 > Flashcards

amboss 7/10 Flashcards

1
Q

what can occur with B12 def

A

subacute combined degeneration of the spinal cord

presents as decreased vibratory sensation at first. macrocytic anemia

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2
Q

what causes the demyelination in B12 def

A

reduced fatty acid synthesis

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3
Q

what is the heterophile antibody test

A

when the serum from a patient is mixed with a horse it aggregates. this is the test for EBV

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4
Q

treatment for Epstein barr

A

fluids, analgesics, antipyretics. watch for splenic rupture for at least 3 weeks after the onset of symtopsm

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5
Q

what is the treatment for rickets

A

sunlight, vitamin D and calcium supplmentation.

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6
Q

what is osteomalacia

A

disorder of impaired mineralization of osteoid. this is essentially adult rickets. usually presents with bone pain and tenderness. leads to bending and pathological fractures

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7
Q

what is rickets

A

a disorder of impaired mineralization of cartilaginous growth plates. usually presents with boney deformities. leads to bending and pathological fractures

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8
Q

what are the labs for osteomalacia and rickets

A

Calcium ↓
Phosphate ↓
Alkaline phosphatase ↑
Parathyroid hormone ↑

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9
Q

what is the treatment for cyanide poisoning

A

hydroxycobalamin

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10
Q

what is the treatment for carbon monoxide

A

100% o2 nasal cannula, or hyperbaric oxygen

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11
Q

what is the presnetation of carbon monoxide poisoning

A

hypertension, confusion, agitation, unsteady gait, short-term memory loss, headache

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12
Q

what is the treatment for reactive arthritis

A

NSAIDs, glucocorticoids, sulfasalazine or MTX

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13
Q

what is reactive arthritis

A

post infectious autoimmune disorder due to gonococcal or chlamydial infections
OR Post-enteritis: after infection with Shigella, Yersinia, Salmonella, or Campylobacter

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14
Q

what can happen to the palms and soles of reactive arthritis

A

they can get hyperkeritinization and lesions that look like nodules

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15
Q

what is leukocytoplastic vasculitis

A

umbrella term for vasculitides, including Henoch-Schönlein purpura (HSP). HSP is an acute immune-complex mediated vasculitis of the small vessels that is often preceded by an upper respiratory infection.

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16
Q

Henoch-Schönlein purpura (HSP) presentation

A

HSP can also manifest with bloody stools or occult bleeding Renal disease is seen in up to 50% with features of nephritic syndrome (e.g., hematuria, proteinuria),

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17
Q

Henoch-Schönlein purpura (HSP) labs

A

↑ Platelet count which is most telling feature.
↑ IgA in serum
↑ Creatinine and/or BUN
Urinalysis to assess possible renal disease
Hematuria, often with RBC casts
Possibly proteinuria
↑ Inflammatory markers

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18
Q

what are the skin findings and kidney damage from HSP mediated by

A

IgA and C3 deposition

mesangial IgA deposition is the hallmark

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19
Q

how to diagnose hemochromatosis

A

genetic testing for C282Y or H63D

liver biopsy used to be the test of choice, now it is confirmatory

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20
Q

what is the presentation of hemachromatosis

A

a high ferritin and a transferrin saturation, especially in the presence of diabetes, hepatomegaly, and hyperpigmentation.
iron accumulates in the heart, pancreas and liver causing end organ damage through cardiomyopathy, cirrhosis, diabetes

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21
Q

what is the treatment for lyme in children under 8

A

amoxicillin; but can use doxycycline if the treatment course is short <21 days
never pick tetracycline

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22
Q

is the screening test for Lyme disease.

A

ELISA Peripheral facial nerve paralysis is the most common cranial neuropathy in Lyme disease. If ELISA is positive, Western blot should be performed to confirm the diagnosis.

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23
Q

the first-line treatment for Lyme carditis associated with arrhythmias

A

Intravenous ceftriaxone,

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24
Q

patient went on a hunting trip recently and now has fever, myalgia, periorbital edema, splinter hemorrhages, eosinophilia, and an increased serum creatine kinase concentration, all of which suggest an infection with

A

Trichinella spiralis.

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25
Q

first-line treatment for primary Raynaud’s phenomenon

A

Calcium channel blockers (particularly nifedipine) are the.

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26
Q

what is tick paralysis

A

rare cause of ascending paralysis caused by a neurotoxin produced in the tick’s salivary gland, which prevents acetylcholine release at the neuromuscular junction. Symptoms typically occur within 2–7 days. Patients present with rapid ascending paralysis (over 24–48 hours) and ataxia, though mental status remains intact.

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27
Q

what is the treatment for tick paralysis

A

removing the tick and assisting with breathing

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28
Q

Major criteria for rheumatic fever

A

include arthritis (migratory polyarthritis primarily involving the large joints), carditis (pancarditis, including valvulitis), sydenham chorea (CNS involvement), subcutaneous nodules, and erythema marginatum.

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29
Q

Minor criteria for rheumatic are

A

arthralgia, fever, ↑ acute phase reactants (ESR, CRP), and a prolonged PR interval on ECG

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30
Q

diagnose rheumatic fever what criteria need to be met

A

two major, or one major plus two minor Jones criteria are required.

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31
Q

what do you give for rheumatic fever treatment

A

penicillin or amoxicillin are the treatments of choice.
if they cannot be given due to sensitivities, use a macrolide such as clarithromycin
must include bed rest and NSAIDs

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32
Q

what is argyll-robertson pupil

A

when the eyes do not react to light, but they still accommodate

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33
Q

what is the cutoff for a positive TB skin test

A

greater than or equal to 5mm in immunocompromised, those with a positive chest X ray, or prior infection or in contact with a known infection

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34
Q

what is the normal urine sodium excretion

A

> 20mEq/L

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35
Q

what is concentrated urine measurement

A

> 100mOsm/kg

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36
Q

what is the best indicator of inadequate fluid resuscitation

A

there should be a urine output of 35-75 ml/hour

urine output in adults should be greater than 0.5 mL/kg/hr

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37
Q

secondary hyperparathyroid is commonly caused by what and why

A

Chronic kidney disease (CKD),

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38
Q

what is the mechanism of secondary hyperparathyroid from CKD

A

decreased levels of serum calcium from impaired renal reabsorption and increased serum phosphate from impaired renal excretion cause reactive hyperplasia of the parathyroid glands, increasing PTH secretion. kidney disease decreases biosynthesis of vitamin D, causing hypocalcemia and a further reactive increase in PTH secretion.

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39
Q

how do we treat hyperphosphatemia

A

sevelemer –a phospohate binding agent

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40
Q

what is good antibiotic coverage for burn victims and why

A

vancomycin and cefepime

staph and pseudomonas

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41
Q

what is empiric treatment of hospital acquired pneumonia

A

vancomycin and cefepime

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42
Q

can you give phentermine to someone with drug use history

A

no.

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43
Q

what is the treatment for low calcium

A

calcium gluconate

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44
Q

what is treatment for a patietn with twitching, abdominal pain, diarrhea, and low PTH

A

calcium gluconate because they are probably low on calcium.

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45
Q

what does multiple blood transfusions put you at risk for

A

hypocalcemia from the citrate in the blood products.

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46
Q

what is always the next step after central line insertion

A

chest x ray to check for proper placement

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47
Q

checking someone blood pressure is a good way to assess what

A

their calcium status

if there is spasm then they have hypocalcemia

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48
Q

when you are thinking about alcoholics and calcium also think of

A

magnesium
hypomagnesiumia is a cause of hypocalcemia becuase it desensitizes PTH
vitamin D deficiency from malnutrition and alcohol-induced increase in urinary excretion of magnesium.

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49
Q

what is the combination of parameters in hypovolemic shock

A

↓ CO, ↓ PCWP, ↑ SVR, and ↓ CVP
There will be blood loss, thus decreased CVP. this will decrease the blood return to the heart and thus the cardiac output will decrease. as this occurs the systemic VR will spike to attempt and maintain BP.
decreased blood delivery to the heart also decreases PCWP

50
Q

the pulmonary capillary wedge pressure is what

A

the left atrial pressurte

51
Q

what is the central venous pressure correlated with

A

blood volume

52
Q

why does the CO decrease in hypovolemia

A

because there is no blood to pump

53
Q

in patients with tissue damage what happens when you administer succinylcholine

A

they go into cardiac arrhythmia because of hyperkalemia

54
Q

what is the presentation of giant cell arteritis

A

oral prednisone and temporal artery biopsy

55
Q

Do you give oral or IV steroids to someone with suspected giant cell arteritis

A

oral if they DO NOT have neurological symptoms and IV methylprednisolone if they do

56
Q

what is the most common cause of gallbladder mets

A

malignant melanoma -the met is often an incidental finding before the primary tumor is even found

57
Q

what is neurogenic shock

A

a distributive shock characterized by generalized vasodilation (causing diaphoresis and flushed skin). This vasodilation leads to decreased preload and subsequently reduced cardiac output, which results in severe hypotension. Bradycardia results from lack of beta adrenergic activity and is exacerbated by unopposed vagal tone.

58
Q

what is SLUDGE and the cause

A

salvation, lacrimation, ,urination, diarrhea,

cholinergic hyperstimulation

59
Q

what is the treatment for cholinergic toxidrome

A

atropine; it should be doubled until bronchial secretions and wheezing stop.
pralidoxime and benzodiazepines should be used as well. .

60
Q

wha tis the mechanism of pralidoxime

A

reactivates acetylchlolinesterase

61
Q

Polymyalgia rheumatica is highly associated with

A

giant cell arteritis, as ∼50% of patients with GCA have PMR, and ∼15% of patients with PMR will have GCA.

62
Q

what is the treatment for acute intermittent porphyria

A

Hemin therapy

heme arginate
glucose loafing

63
Q

what is the presentation of acute intermittent porphyria

A

(Painful abdomen, Polyneuropathy, Psychologic disturbances, Precipitated by drugs/alcohol, and Purple pee).
Fever
GI symptoms: severe abdominal pain, nausea, vomiting
Neurological abnormalities
Polyneuropathy: non-specific pain, weakness/fatigue, paresthesia, paresis
Seizures
Psychiatric abnormalities: hallucinations, disorientation, anxiety, insomnia
Autonomic dysfunction: tachycardia, hypertension
Red-purple urine

64
Q

what blood disorder can a partial gastrectomy cause and why

A

macrocytic anemia due to loss of parietal cells that bind intrinsic factor.

65
Q

Lambert-Eaton myasthenic syndrome (LEMS)

A

autoantibodies against the P/Q voltage-gated calcium channels at the presynaptic motor neuron

66
Q

what causes heat stroke in elderly adults

A

inadequate hypothalamic thermoregulatory response

67
Q

what is the SE of metaclopramide

A

Adverse effects include extrapyramidal symptoms (e.g., dystonia), likely secondary to dopamine antagonism.

68
Q

what are the characteristics of patau

A

trisomy 13 rocker bottom feet, polydactyly. cleft lip and palate, cloumboma, small jaw, small eyes, low set ears. microcephaly

69
Q

charateristics of Edwards

A

trisomy 18 Characteristic features include clenched fists with flexion contractures of the fingers, rocker-bottom feet, a prominent occiput, and visceral malformations (e.g., horseshoe kidneys). Further features may include low-set ears, micrognathia, and a cleft lip and palate.

70
Q

what is the presentation of wiskott Aldrich syndrome

A

X-linked that is characterized by eczema, thrombocytopenia and immune dysfunction

71
Q

what is fanconi anemia

A

autosomal recessive disorder caused by a heterogeneous group of mutations, all of which lead to deficits in DNA repair mechanisms and, thus, a high frequency of chromosomal aberrations.One of the most common and notable features is a predisposition for developing acute myeloid leukemia or myelodysplastic syndromes in early adulthood. short stature, hypopigmentation and hyperpigmentation of the skin, cafe-au-lait spots, microcephaly and developmental delay, ocular abnormalities including esotropia and hypertelorism, and thumb and forearm malformations.

72
Q

what is the residual volume for CF patients

A

increased due to obstructive lung disease and air trapping, usually

73
Q

what is the acid base disorder most commonly found in CF patient

A

chloride dependent metabolic alkalosis

74
Q

what is the coagulation cascade finding most likely to be found in CF patients

A

elevated PT time due to loss of vitamin K and

75
Q

what diseases do CF patients most likely get

A

98% have infertility due to a lack of a vas deferens. they will usually develop CF-related diabetes

76
Q

what is leach nyhan sydnrome caused by a

A

mutation of hypoxanthine-guanine phosphoribosyltransferase (HGPRT), an enzyme involved in purine metabolism.

77
Q

what is cystathionine synthase deficiency

A

presentation of Marfanoid habitus, high-arched palate, inferior lens dislocation, kyphosis, hyperelastic skin, hypermobile joints, and possibly intellectual disability (as indicated by delayed language, block-building, and drawing abilities).

78
Q

what is the test for cystinuria

A

nitroprusside

79
Q

what is the treatment for cystinuria

A

B6 abd B12

80
Q

do we need molecular testing for marfan

A

no, it is a clinical diagnosis. we can use it to confirm.

81
Q

what is one of the first and most important tests to do on someone with Marfan

A

echo for MVP and other cardiovascular manifestations

aortic root dilation/aortic aneurysm/aortic dissection

82
Q

what do you use to treat Kawasaki

A

IVIG and high dose aspirin

83
Q

what is the proper course for alkaline ingestion

A

remove all clothes, inspect mouth, can intubate and ventilate, upper endoscopy to assess the extent of the burn

84
Q

what can happen when you are immobile and what is the treatment

A

increased calcium, phosphorus and alk phos

bisphosphonates

85
Q

The pathophysiology of HELLP syndrome

A

overactivation of the coagulation cascade.

86
Q

Up to 50% of cases of hepatocellular carcinoma (HCC) occur secondary to

A

chronic hepatitis B infection. Although the majority of such cases (∼ 80%) are preceded by liver cirrhosis, HCC can also arise directly from chronic HBV infection

87
Q

what is persistent depressive disorder (dysthymia

A

depressive mood for more than 3 years not due to substance use and only having one month of normal behavior at a time

88
Q

what is associated with pagets

A

reduced hearing

89
Q

what is a bone sequestrum and what is it associated with

A

osteomyelitis -a dead separated piece of bone

90
Q

what is the presentation of pagets

A

bone deformities occur often. markedly elevated PTH with normal calcium and phosphorus
reduced hearign

91
Q

what is the treatment for good pastures

A

emergent plasmapheresis, steroids and cyclophosphamide

92
Q

what is the normal liver span at the midclavicualr line

A

6-12 cm

93
Q

what is highly associated with systemic sclerosis

A

lung cancer. 5X higher risk

94
Q

what is CREST

A

calcinosis cutis, Raynaud, esophageal hypomotility, sclerodactyly, telangiectasia

95
Q

what is the presentation of systemic sclerosis

A

pulmonary fibrosis, sclerodactyly and Raynaud, arthralgia, scleroderma, GERD, dysphagia, microstomia, telangiectasia,

96
Q

what is anticentromere antibodies diagnostic for

A

CREST, a type of limited systemic sclerosis

97
Q

what type of lung disease do people with ankylosing spondylitis have and how does it differ from the normal presnetation

A

restrictive, but slightly different, as the functional residual capacity and the RV are normal

98
Q

what is the lung function panel for someone with restrictive lung disease

A

decreased forced vital capacity, decreased or normal FEV1

99
Q

vitamin A toxicity l

A

Acute toxicity presents with headache, fatigue, dizziness, nausea, loss of appetite, dry skin, alopecia, and possibly cerebral edema. Chronic intoxication may further present with osteoporosis, bone pain, and psychiatric changes

100
Q

what is there presentation of zinc deficiency

A

scaly skin, alopecia, –most commonly in alcoholic

101
Q

what is porphyria cutanea tarda

A

an acquired or genetic disease of blistering of the skin due to triggers such as sunlight. defective uroporphyrinogen-III decarboxylase (UROD) which leads to the accumulation of uroporphyrinogen in the skin and chronic photosensitivity with blistering and hyperpigmentation.

102
Q

what is the treatment for porphyria cutanea tarda

A

phlebotomy and hydroxychloroquine

103
Q

what is the presentation of polyarteritis nodosum

A

erythematous nodules, malaise, night sweats, arthralgia, anemia, leukocytosis, and elevated ESR and CRP. However, decreased radial/pedal pulsations are typically not present because peripheral vascular disease is a rare manifestation of PAN. Instead, patients usually present with hypertension and/or renal insufficiency (due to renal artery stenosis) and symptoms of neuropathy (e.g., paresthesias, sensory loss, weakness).

104
Q

Takayasu arteritis

A

is a granulomatous inflammation involving all layers of the walls of large arteries such as the aorta and its major branches. Its incidence peaks at 15–45 years of age and it is more common in women (especially those of Asian ethnicity). In the initial stages of the disease, patients have nonspecific symptoms such as fever, malaise, and/or arthralgia. Eventually, the large arteries narrow, which causes the peripheral pulses to decrease in strength. Systemic inflammation causes elevation of ESR, CRP, leukocyte count, and thrombocyte count. In some patients, a necrotizing inflammation of medium-sized subcutaneous vessels occurs, which results in erythema nodosum.

105
Q

what is the first step in determining proper treatment for raynauds

A

serological testing

106
Q

what is polyarteritis nodosum associated with

A

hepatitis B

107
Q

what electrolyte abnormality is found in sarcoidosis and why

A

hypercalcemia because of macrophages within the noncaseating granulomas releasing vitamin D

108
Q

what is likely to found in someone with a chronic hep C infection that has a pruritic rash

A

hypocomplementemia

109
Q

what type of cardiomyopathy does coxsackie B myocarditis cause

A

dilated

110
Q

what is microscopic polyangiitis

A

chronic cough and hemoptysis in addition to nonspecific symptoms such as fatigue, myalgia, and weight loss. Skin lesions such as palpable purpura are also a common feature. A biopsy of the involved organ (usually the skin or kidney) helps to confirm the diagnosis. A kidney biopsy would show little or no immune deposits (pauci-immune glomerulonephritis).

111
Q

what antibodies are found in microscopic polyangiitis

A

Perinuclear antineutrophil cytoplasmic autoantibodies (p-ANCA), specifically anti-MPO (myeloperoxidase) antibodies are positive in 90% of patients with microscopic polyangiitis (MPA).

112
Q

what antibodies are associated with polymyalgia rheumatica

A

none

113
Q

what are the findings in polymyalgia rheumatica

A

shoulder and hip girdle tenderness, non erosive arthritis, carpal tunnel. morning stiffness. ↑↑ ESR, specifically > 50 mm/h
↑ CRP
Leukocytosis
Normochromic anemia
Normal creatine kinase, negative rheumatoid factors and no autoantibodies
Bursitis on ultrasound of affected joints

114
Q

do we take a muscle biopsy for polymyalgia rheumatica

A

no.

115
Q

what is the treatment for polymyalgia rheumatica

A

oral prednisone

116
Q

what is associated with dermatomyositis and why

A

ovarian, gastric cancer and lymphoma, elevated CA-125 levels if ovarian cancer is there

117
Q

what is a way to confirm orthostasis

A

BUN/Creatinine elevated BUN from hypoperfusino

118
Q

what bone problem is seen in 50% of cushings

A

osteoporosis there is an increased risk of fractures and avascualr necrosis of the femoral herad

119
Q

what large vessel pathology is associated with giant cell arteritis

A

thoracic aortic aneurysm

120
Q

what is the presentation of nitroprusside poisoning and why the fuck would you ever treat someone with this

A

hypertensive crisis.
confusion, headache, flushed skin, bright red retinal veins, and anion gap lactic acidosis is suggestive of cyanide poisoning.f

121
Q

what do you treat ankylosing spondylitis with

A

Consistent and rigorous physical therapy
Independent exercises
Medical therapy
First choice: NSAIDs (e.g., indomethacin)
Additional options
Tumor necrosis factor-α inhibitors (e.g., etanercept, adalimumab) [12]
In case of peripheral arthritis: DMARDs (especially sulfasalazine)
In severe cases: temporary, intra-articular glucocorticoids

122
Q

what are strict vegans at risk for

A

low bone mineral density due to diminished calcium

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