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Internal Med > firecracker feb 12 > Flashcards

firecracker feb 12 Flashcards

1
Q

erythema multiforme infectious causes

A

HSV

Mycoplasma pneumoniae

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2
Q

what is erythema multiforme

A

acute cutaneous hypersensitivity condition
immune mediated
target like lesions

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3
Q

erythema multiforme most common among

A

males

20-40

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4
Q

erythema multiforme other findings besides target lesions

A

malaise, mylagias
macules
plaques, vesicles

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5
Q

erythema multiforme lesions

A

red center
pale inner ring
red outer ring

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6
Q

meds linked to erythema multiforme

A

penicillins

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7
Q

erythema multiforme diagnosis

A

skin biopsy
increased lymphocytes
necrotic keratinocytes

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8
Q

erythema multiforme treatment

A

stop offending agent
corticosteroid
analgesics

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9
Q

how does membranous nephropathy present

A

edema

dyspnea

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10
Q

risk factors for autoimmune hepatitis

A

caucasian/northern europe
female
acute hep a and b infections
DR3,4

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11
Q

membranous nephropathy treatment

A

corticosteroids, cytotoxic agents, statins, ACEI

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12
Q

lab findings in membranous nephropathy

A

hyperlipidemia
hypoalbuminemia
proteinuria

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13
Q

What is the role of anticoagulation in the management of membranous nephropathy?

A

increase in coagulopathies

severe proteinura >5g/day

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14
Q

autoimmune hepatitis serological

A

Anti smooth muscle

anti live rkidney microsomal

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15
Q

autoimmune hepatitis treatment

A

prednisone

azathioprine

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16
Q

membranous nephropathy - immunoflourescnce

A

granular deposits of IgG and C3

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17
Q

What is found on electron microscopy in patients with membranous nephropathy?

A

sub-epithelial immune complex deposits

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18
Q

secondary membranous nephropathy

A

hep b, c
autoimmune - lupus
drugs - gold, penicillaine
malignancies

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19
Q

autoimmune hepatitis

A

circulating antibodies
hepatocellular inflamm
fibrosis

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20
Q

follicular carcinoma %

A

15%

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21
Q

what is the first and second step in working up someone with a thyroid nodule?

A
  • ultrasound (FNA)
  • radionucleotide scan if suspicious
  • biopsy
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22
Q

What percentage of thyroid CA’s are from a medullary carcinoma?

A

5%

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23
Q

medullary carcinoma - cells

A

parafollicular/C cells

produce calcitonin

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24
Q

How does follicular thyroid CA commonly spread?

A

hematogenous spread –> present with mets

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25
Q

thyroid CA treatment

A

surgical removal
radioactive iodine ablation
lobectomy if less than 1cm
total thyroidectomy if greater than 1 cm

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26
Q

What medication is started post-operatively for patients who have undergone surgery for thyroid cancer?

A

levothyroxine

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27
Q

What is the most common sub-type of thyroid CA?

A

papillary

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28
Q

What is a common history in patients who develop papillary thyroid CA? How does it spread?

A

exposure to ionizing radiation

spreads thru lymphatics

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29
Q

prolactinoma signs & symptoms

A

F: galactorrhea, amenorrhea
M: loss of libido, erectile dysfxn, gyecomastia

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30
Q

prolactinoma =

A

hyperfunctioning adenoma of anterior pituitary

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31
Q

hormones secreted from anterior pituitary

A

My FLAT PiG

MSH, FSH, LH, ACTH, TSH, Prolactin, GH

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32
Q

prolactinoma treatment

A

bromocriptine or cabergoline —> dopamine agonists

dopamine inhibits prolactin release

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33
Q

other causes of hyperprolactinemia

A

pregnancy
drugs
hypothyroid/hypothalamic damage

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34
Q

causes of central DI

A

idiopathic
trauma
tumors
anorexia

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35
Q

diabetes insipidus

A

can’t retain water

water normally retained by reabsorbing it from urine

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36
Q

DI symptoms

A

polyuria, polydipsia, new onset nocturia

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37
Q

First Step Of workup for DI

A

urinarlysis
dilute urine, urine osm less than serum osm (290)
urine specific grav less than 1.06

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38
Q

causes of nephrogenic DI

A

hereidtary renal diseases
lithitum toxicity
hypokalemia
hypercalcemia

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39
Q

second step of DI workup

A

water deprivation test

no change in urine osm after water deprivation

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40
Q

DDAVP test

A

increased urine osm in central

no change in nephrogenic (renal resistance to ADH)

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41
Q

central DI treatment

A

desmopressin

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42
Q

nephrogenic DI treatment

A

underlying disorder

symptoms with hctz, indomethacin, amiloride

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43
Q

secondary adrenal insufficiency most commonly caused by

A

glucocorticoids

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44
Q

What infective infiltrative disorders may affect the adrenal glands?

A

TB
Histo
HIV

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45
Q

secondary adrenal insufficiency

A

failure of HPAxis

decreased ACTH

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46
Q

What pituitary neoplasms commonly suppress ACTH production?

A

pituitary adenoma

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47
Q

What are some causes of adrenal insufficiency?

A
  • autoimmune destruction
  • Tb, Hiv
  • infarction of adrenal gland
  • Waterhouse-Friderichsen
  • DIC
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48
Q

what is low in adrenal insuffieiency

A

low morning cortisol, less than 5

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49
Q

What is a common cause of adrenal insufficiency in patients in a hypercoagulable state or in sepsis?

A

hemorrhagic adrenal infarction

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50
Q

What hormones are secreted by the adrenal cortex?

A

aldosterone
cortisol
androgen

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51
Q

What is “stress dosing” of steroids and when is it indicated in adrenal insufficiency?

A

increased doses given in cases of stress like infection or surgery

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52
Q

What may precipitate adrenal crisis?

A

stress - surgery, sepsis

look for hypotension, hyponatremia, hyperkalemia

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53
Q

What replacement therapy is needed in patients with primary adrenal failure in addition to prednisone?

A

aldosterone with fludrocortisone

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54
Q

What is the cosyntropin test and what would be considered an abnormal result?

A

differentiate 1 vs 2 ACTH def
ACTH analog
cortisol > 20 normal result
lower indicates non response, primary adrenal failure

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55
Q

What is a common life-threatening complication of adrenal insufficiency?

A

shock (adrenal crisis)

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56
Q

treatment for adrenal crisis

A

IV glucose and corticosteroids

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57
Q

What test is used to confirm acromegaly if IGF-1 are found to be elevated?

A

ORAL glucose tolerance test

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58
Q

What are two important metabolic complications of acromegaly?

A

DM

HLD

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59
Q

What can be used to treat persistent elevations in insulin growth factor 1 after transphenoidal resection of the growth hormone secreting pituitary adenoma?

A

radiation therapy

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60
Q

What constitutes an abnormal oral glucose tolerance test in patients with acromegaly?

A

GH remains greater than 2 within two hours after ingestion of 75g glucose

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61
Q

Patients who have been diagnosed with acromegaly based on elevated IGF-1 levels and positive glucose tolerance test require what further testing?

A

MRI of brain

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62
Q

What is the cause of obstructive sleep apnea in acromegaly?

A

GH causing macroglossia

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63
Q

acromegaly rx

A

somatostatin and dopamine analogues such as ocretotide and bromocriptine

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64
Q

CNS symptoms of acromegaly

A

bitemporal hemianopsia

headaches

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65
Q

body parts affected by acromegaly

A

hands, skull, jaw

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66
Q

cause of primary hyperPTH

A

single benign adenoma

hyperplasia of parathyroid glands

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67
Q

triad of primary hyper PTH

A

hypercalcemia
elevated PTH
elevated 24 hr urinary calcium

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68
Q

secondary hyperPTH

A

parathyroid glands chronically stimulated by hypocalcemia to release PTH

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69
Q

how does primary hyperPTH present

A

hypercalcemia

bones, stones, moans, groans, polyuria

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70
Q

causes of secondary hyperPTH

A

CKD
Malabsorption
Rickets
PseudohyperPTH

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71
Q

indications for surgical intervention in primary hyperPTH

A

elevated cr
hypercalcemia
kidney stones
osteoporosis

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72
Q

secondary hyperPTH labs

A

low calcium, high phosphorus

high PTH

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73
Q

cortisol production

A

hypothalamus produces CRH
pituitary produces ACTH
ZF of adrenal gland produces cortisol

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74
Q

what test to determine ACTH-independent vs ACTH-dependent cushing’s

A

plasma ACTH

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75
Q

what causes glucose intolerance in Cushing’s?

A

cortisol-stimulated gluconeogenesis

obesity-induced peripehral insulin resistance

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76
Q

How does a low-dose dexamethasone suppression test help diagnose Cushing’s syndrome?

A

normal morning cortisol following dexa should be s

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77
Q

Complications of cushing’s

A

diabetes
CVD
opportunistic infections

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78
Q

imaging in cushings

A

look for source

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79
Q

infections in Cushing’s syndrome

A

Nocardia
PCP
fungal

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80
Q

skin in Cushing’s

A

thinning
bruising
striae
hyperpigmentation

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81
Q

acne in Cushings?

A

imablance in adnrogens, estogren, GnRH

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82
Q

osteoporosis in Cushings?

A

reduced calcium absorption in intestines and kidneys

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83
Q

lab abnormalities in Cushings

A

hypokalemia
hypercalciuria
metabolic alkalosis

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84
Q

Cushings work up

A

24 urinary free cortisol test (3x)

low dose dexamethasone suppresion test

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85
Q

Cardiogenic Shock

A

decrease CO
increase SVR
increase PCWP

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86
Q

Hypovolemic Shock

A

decrease CO
increase SVR
decrease PCWP

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87
Q

Neurogenic Shock

A

decrease CO
decrease SVR
decrease PCWP

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88
Q

Septic Shock

A

increase CO
decrease SVR
decrease PCWP

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89
Q

Pharmacologic Agents in Cardiogenic Shock

A

Dopamine - vasopressor

Dobutamine - inotrope

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90
Q

Shock =

A

circulatory collapse

inadequate blood delivery resulting in hypoperfusion of tissues

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91
Q

How is anaphylactic shock managed?

A

airway maintenace
epinephrine
diphenhydramine
IV fluids

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92
Q

cardiogenic shock defined as

A

hypotension below 80-90 or 30mmhg below baseline

urine output less than 20 ml/hr

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93
Q

causes of cardiogenic shock

A 
acute mi
arrhythmias 
tension PTX
cardiac tamponade
massive PE
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94
Q

neurogenic shock =

A

SNS failure causing widespread peripheral vasodilation and bradycardia

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95
Q

anaphylactic shock =

A

type I hypersenisitivty rxn

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96
Q

etiology of neurogenic shock

A

CNS or spinal cord injury

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97
Q

cardiogenic shock =

A

heart fails to generate sufficient CO to perfuse tissues

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98
Q

causes of hypovolemic shock

A

hemorrhage

excess fluid loss

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99
Q

cause of anaphylactic shock

A

massive degranulation of mast cells and basophils in response to allergic rxn

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100
Q

management of neurogenic shock

A

IV fluids, vasoconstrictors to treat vasodilation

atropine for braycardia

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101
Q

management of hypovolemic shock

A

IV fluids or transfusions
surgery
dressing if due to burns

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102
Q

hemodynamic effects of cardiogenic shock

A

decrease in SV

increase in EDP and ESV

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103
Q

cardiogenic shock - PE findings

A

JVD, pulm edma
AMS
cool, clammy skin
weak thready pulse

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104
Q

management of shock related to MI

A

revascularization

use of aspirin and heparin

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105
Q

clinical features of neurogenic shock

A

warm, well perfused skin

low-normal urine output

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106
Q

symptoms of ARDS - focus on breath sounds

A

wheezing
rales
rhonchi

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107
Q

ARDS

A

acute lung inury
complement activation –> lung damage
refractory hypoxemia

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108
Q

PaO2/FiO2 ratio for ARDS

A

<200

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109
Q

ARDS lab findings

A

resp alkalosis
decrease o2
decrease co2

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110
Q

causes of ARDS, A

A

aspiration
acute pancreatitis
air or amniotic embolism

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111
Q

causes of ARDS, R

A

radiation

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112
Q

causes of ARDS, D

A

drug over dose
DIC
drowning

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113
Q

causes of ARDS, s

A

shock
sepsis
smoke inhalation

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114
Q

CXR for ARDS

A

bilateral pulmonary edema with infiltrates

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115
Q

BCC risk factors

A

p53, HPV

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116
Q

BCC

A

most common

sun exposed areas

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117
Q

BCC lesion

A

pearly, waxy apperance

telangiectases throughout lesion

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118
Q

BCC diagnosis

A

skin biopsy

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119
Q

BCC treatment

A 
electrodessication and curettage
surgical excision
cryotherapy
topical meds
radiation therapy
120
Q

BCC - meds

A

5FU
imiquimod
tazarotene

121
Q

BCC -radiation

A

extensive dz

can’t undergo surgery

122
Q

SCC risk factors

A

HPV

actinic keratosis

123
Q

SCC lesion

A

scaly, ulercated skin lesion

shallow ulceration with healed up borders

124
Q

gold standard for diagnosing melanoma

A

excisional skin biopsy with a 1-2mmof normal appearing skin

125
Q

melanoma complications

A

scarring, keloid formation, metastasis, death

126
Q

cause of dehydration in HHNK

A

increased blood glucose –> increased insulin demand –> increased plasma osm –> osmotic diuresis –> dehydration

127
Q

HHNK lab values

A

elevated glucose, 600+
elevated plasma osmolality, +350
no ketones

128
Q

potassium levels in HHNK

A

normal despite low total-body stores

129
Q

what prevents ketoacidosis in HHNK

A

some circulating insulin which prevents lipolysis

130
Q

HHNK ABG

A

normal ph, normal bicarb

131
Q

HHNK presentation

A

polydipsia, polyuria, AMS, dehydration

132
Q

Cr in HHNK

A

prerenal azotemia

133
Q

HHNK treatment

A

NS
Insulin
glucose
potassium

134
Q

when glucose reaches 250-300 in HHNK

A

given 5% dextrose

135
Q

Hemophilia A

A

Factor 8 def

136
Q

Hemopihilia A&B inheritance patterns

A

x linked recessive

137
Q

hemophilia lab values

A

prolonged PTT

138
Q

hemophilia symtpoms

A

hemarthroses (bleeding into joints)

intramuscular hematomas

139
Q

Hemophilia B

A

def of Factors 9

140
Q

Hemophilia A treatment

A

Factor 8 during acute bleeding episodes

minor dz, DDAVP

141
Q

Hemophilia B treatment

A

factor 9 concentrates

not DDAVP

142
Q

coccidiomycosis treatment

A

self resolving

143
Q

coccidiomycosis skin findings

A

genearlized macular erthematus eruption of eryhthema nodosum

144
Q

coccidiomycosis symptoms

A

fevers/chills/night sweats

chest pain

145
Q

coccidiomycosis symptom constellation

A

erythema nodusum, fever, chest pain, arthrlagias

146
Q

extrapulmonary sites of TB

A

meningitis

potts - bones of spine

147
Q

Tb treatment

A

RIPE for 2 months

4 months of isoniazid & rifampin

148
Q

asymptomatic TB treatment

A

isoniazid for 9 months

149
Q

Tb test - 5mm induration

A

HIV positive
close contact
CXR changes
immunosuppression

150
Q

gastritis triggers (3)

A

alcohol
nsaid
h pylori

151
Q

gastritis - best diagnostic study

A

upper endoscopy with mucosal biopsy

152
Q

gastritis - determining extent of erosions

A

double contrast barium study

153
Q

gastritis - lab tests

A

CBC
stool guiac
stool antigen and urea breath test

154
Q

CKD most common causes

A

HTN
DMT2
Glomerulonephritis

155
Q

stage III CKD

A

30-59

156
Q

5 absolute indications for emergent dialysis in CKD

A 
acidosis
electrolyte abnormalities
ingestion of toxins
overload of fluid
uremia
157
Q

stage V CKD

A

less than 15

158
Q

CKD sodium and water retention

A

HTN, accelerated atherosclerosis
peripheral edema
CHF

159
Q

Renal Osteodystrophy in CKD

A

hyperphosphatemia stimulates PTH
decreased alpha1vit D causes increased PTH
low calcium
osteitis fibrosis cystica

160
Q

treatment of CKD anemia

A

EPO stimulating agents (can increase BP & thrombotic risk)

161
Q

Stage IV CKD

A

15-29

162
Q

CKD anemia

A

decreased EPO

normochromic, normocytic anemia

163
Q

CKD labs

A 
elevated Bun, CR
increase K, phosphate
decreased Na, Ca
anemia
metabolic acidosis
164
Q

volume managemnt in CKD

A

loop diuretics

165
Q

CKD anion-gapped metabolic acidosis

A

decreased excretion of H ions in ammonium

decreased renal excretion of organic anions

166
Q

hyperkalemia in CKD

A

inability to excrete potassium

167
Q

platelet dysfunction in CKD

A

uremia-induced

increased bleeding risk

168
Q

CKD increased infection risk

A

uremia-induced neutrophil dysfunction

169
Q

CKD metabolic acidosis treatment

A

sodium bicarb

170
Q

CKD stage 1

A

90+

171
Q

CKD dietary modifications

A

low phosphate diet, phosphate binders
vit d analogues
low potassium diet
protein restriction

172
Q

CKD stage II

A

60-89

173
Q

treatment of AIN

A
  • supportive

- corticosteroids

174
Q

AIN presentation

A

ARF w/

fever, rash, N/V, malaise

175
Q

AIN lab values

A

increase in Cr

eosinophilia

176
Q

AIN caused by what toxins?

A 
cadmium
lead
copper
mercury
mushrooms
177
Q

AIN caused by what drugs?

A

Pencillin, NSAID, Allopurinol, Diuretics, Cephalosporins, PPI, Sulfonamide/Sulfasalazine, Rifampin

178
Q

AIN caused by systemic diseases?

A

Strept, Legionella
Sarcoidosis, Amyloidosis,
SLE
Myoglobinuria, high uric acid levels

179
Q

AIN urinalysis

A

granual and epithelial casts

180
Q

AIN kidney biopsy

A

inflamm cells in interstitium

tubular cell necrosis

181
Q

AIN complications

A

ATN
ARF, CRF
RPN

182
Q

septic arthritis PE findings

A

warm, red, tender joint

skin lesions

183
Q

septic arthritis cause in young male

A

N. gonorrhea

184
Q

septic arthritis- most common pathogen

A

s. aureus

185
Q

septic arthritis in immunocompromised

A

fungal, candida

186
Q

treatment for S. aureus septic arthritis

A

nafcillin/oxacillin/dicloxacillin

187
Q

treatment for N. gonorrhoeae septic arthritis

A

ceftriaxone + axithro/doxy

surrigical irrigation and drainage usually not necessary

188
Q

septic arthritis in sickle cell pts and IV drug users

A

Salmonella

Pseudomonas

189
Q

gram negative septic arthritis treatment

A

aminoglycoside

190
Q

MRI in septic arthritis

A

confirm joint effusion

191
Q

joint aspirate in septic arthritis

A

wbc 50000+
high neutrophil count
low glucose

192
Q

septic arthritis treatment

A

surgical irrigation and drainage

193
Q

septic arthritis - what to monitor for treatment efficacy

A

CRP

194
Q

septic arthritis lab findings

A

WBC 10K+
ESR 30+
CRP 5+

195
Q

septic arthritis symptoms

A

pain in joint
fever
pain with passive ROM

196
Q

Malaria affects which RBCs

A

vivax/ovale: reticulocytes

malariae: mature RBC
falciparum: reticulocytes & RBC

197
Q

malaria vector

A

Anopheles mosquito

198
Q

malaria symptoms

A

chills, myalgia, HA
NVD
splenomegaly

199
Q

hypnozoites associated with

A

vivax/ovale

200
Q

fever & malaria

A

falciparum constant
ovale and vivax - q48hr
marlariae - q72h

201
Q

most severe form of malaria with cerebral, renal & pulm symptoms

A

falciparum

202
Q

primaquine as treatment and prophylaxis for malaria in

A

Mexico and Argentina

203
Q

treatment of malaria in chloroquine resistant areas

A

quinine sulfate + tetracycline
atovaquone-proguanil
artemether-lumefantrine

204
Q

med for Pvivax and Povale malaria

A

primaquine phosphate, two weeks

205
Q

malaria prophylaxis

A

chloroquine

mefloquine

206
Q

malaria diagnosed with

A

perpheral blood smear with giemsa-staining

207
Q

primary syphilis

A

painless chancre (ulcerated penile lesion)

208
Q

4 causes of false positives with VDRL

A

viruses (mono, hepatitis)
drugs
rheumatic fever
lupus and leprosy

209
Q

tertiary syphilis

A

gumma formation
aortitis
neurosyphilis

210
Q

congenital syphilis initial symptoms

A

rhinitis
lesions on palms/soles
HSM, jaundice
hemolytic anemia, thrombocytopenia

211
Q

neurologic symptoms of tertiary syphilis

A

tabes dorsalis
argyll-roberston pupils
broad based ataxia
stroke

212
Q

condyloma lata

A

smooth, flat, lessions in most areas

213
Q

screening test and confirmatory test for syphilis

A

VDRL or RPR

FTA-ABS

214
Q

negative VDRL with positive FTA

A

sucessfully treated syphilis

215
Q

treatment for primary syphilis

A

benzanthine penicillin IM

doxy or tetracycline for 2 weeks

216
Q

treatment of secondary and tertiary syphilis

A

benzathine pencilline g IM for 3 wks

doxy for 28 d

217
Q

three general causes of acquired long QT syndrome

A

drugs
electrolyte imbalance
MI

218
Q

long qt =

A

delayed in repolarization of myocardium

219
Q

What effect does every drug that causes prolongation of the QT interval have?

A

block cardiac Ikr current mediated postassium channels

220
Q

diagnosis of Qt prolong on ECG?

A

qt/sqrt(RR)

less than 440

221
Q

electrolyte imbalances that can cause long qt

A

hypokalemia
hypomagnesium
hypocalcemia

222
Q

drugs that cause long qt

A 
quinidine, amiodarone
haloperiodal, methadone
cisapride
erythromycen
aresenic trioxide
223
Q

prolonged QT life threatening complication

A

torsades de pointes

224
Q

long qt treatments

A

stop drug, correct electrolytes, IV mag sulfate

225
Q

lactase absorbed …

A

brush border of enterocytes

226
Q

borborygmi

A

rumbling noises made by gas and fluid in intestines

227
Q

tests for lactose intolerance

A

lactose absorption test (minimal increase in serum glucose)

lactose breath hydrogen test

228
Q

lactose intolerance stool

A

bulky, frothy, watery

229
Q

lactase deficiecny pathophysiology

A

lactase production decreases over time

injury to small intestine

230
Q

etiologies of DIC

A

1) sepsis
2) trauma
3) malignancy
4) ob complications
5) severe intravascular hemolysis (malaria, AHTR)

231
Q

pathogenesis of DIC

A

1) exposure of excess tissue factor
2) coagulation
3) thrombosis & fibrinolysis
4) hemorrhage

232
Q

chronic DIC clinical manifestations

A

asymptomatic

predilection for thrombosis

233
Q

factors that determine whether DIC will be acute or chronic

A
  • etiology

- rate

234
Q

DIC lab findings

A

1) thrombocytopenia
2) shistocytes
3) decreased fibrinogen, elevated PTT, PT
4) elevated
FDP, D-dimer

235
Q

lab findings in chronic DIC

A

elevated FDPs, D-dimer, schistocytes

no coagulopathies

236
Q

DIC supporative care

A

transfuse platelets if less than 50K

increased INR/decrease in fibrinogen: FFP or cryoprecipate

237
Q

purpura fulminans

A

rate but fatal complication of DIC
extensive tissue thrombosis and skin necrosis
treat with proctein c

238
Q

what predisposes to myxedema coma?

A

longstanding uncontrolled hypothyroidism (usually primary)

239
Q

supportive measures in myxedema coma?

A

intubation with mechanical ventilation
passive rewarming
non-dilute fluids with electrolytes and glucose

240
Q

myxedema coma =

A

severe hypothyroidism
with
decreased MS, hypothermia, hyponatremia

241
Q

What makes airway management challenging in a patient with myxedema coma?

A

nonpitting edema - enlarged tongue, edematous pharynx

242
Q

4 complications of myxedema coma

A

cardiac abnormalities
lipid abnormalities
anemia
depression

243
Q

myxedema coma labs

A

TSH, free T4, cortisol

244
Q

myexedma coma clinical presentation

A

decreased MS
hypothermia
hyponatremia
hypercapnia

245
Q

myxedema cardiac abnormalities

A

low cardiac output, hypotension, CHF

reverse with correction of thyroid hormones

246
Q

drug given during myxedema coma

A

IV levothyroxine (T4)

247
Q

hereditary elliptocytosis genetic mutations

A

eryhtrocye membrane proteins: alpha spectrin, beta spectrin

248
Q

hereditary elliptocytosis more prevalent in africa…

A

protection against malaria

249
Q

primary cause of symptoms in hereditary elliptocytosis

A

hemolytic anemia/chronic hemolysis

250
Q

treatment of hereditary elliptocytosis with severe symptoms

A

splenectomy

blood transfusion

251
Q

most severe type of hereditary elliptocytosis

A

hereditary pyropoikilocytosis

252
Q

best initial treatment for hereditary elliptocytosis

A

no treatment

folic acid

253
Q

6 states that worsen hemolytic anemia in hereditary elliptocytosis?

A 
neonates (high 2,3BPG)
renal allograft rejection
TTP/HUS
infection
pregnancy
b12 def
254
Q

roles of vWF in hemostasis

A

adheres to platelets and subendothelial components

binds favtor VIII

255
Q

vWD diagnostic tests

A

plasma vwf antigen
plasma vwf activity (ristocetin cofactor assay)
factor VIII activity

256
Q

wVD clincial scenarios

A

difficult to control epistaxis
excessive bleeding following invasive procedures
menorrhagia
excessive peripartum bleeding

257
Q

vWD pts before surgery should be given

A

vWF concentrate

258
Q

presenting symptoms of FSGS

A

edema
foamy urine
HTN
dyspnea

259
Q

FSGS risk factors

A

IV drug use

HIV

260
Q

FSGS biopsy

A

sclerotic changes in glomeruli

261
Q

FSGS treatment

A

steroids, cytotoxic agents, ACEI, statins

262
Q

FSGS lab findings

A

HLD, hematuria, high levels of proteinuria, hypoalbuminemia

263
Q

wegner’s biopsy

A

granulomatous inflamm of blood vessels

264
Q

MPGN etiologies

A

Hep B,C
Lupus
bacterial endocarditis
autoimmune, idiopathic

265
Q

MPGN lab findings

A

hematuria

hypocomplementemia

266
Q

osmotic diuresis leading to hypernatremia

A

mannitol

glucosuria

267
Q

renal cell CA triad

A

hematuria
palpable flank masses
flank pain

268
Q

renal cell CA paraneoplastic syndromes

A

PTHrp, EPO, ACTH, Renin

269
Q

causes of hypervolemic hypernatremia

A

cushings
exogenous steroids
primary hyperaldosteronism

270
Q

hypercalcemia ekg findings

A

av block, shortened qt

271
Q

renal sodium loss – hypovolemic hypernatremia

A

diuretics
osmotic diuresis
renal failure

272
Q

extra renal sodium loss – hypovolemic hypernatremia

A

diarrhea, diaphoresis, respiratory

273
Q

good pastures triad

A

anti GBM antibodies
rapidly progressive GN
pulmonary hemorrhage

274
Q

MPGN treatment

A

steroids with aspirin or dipyridamole

275
Q

polyarteritis nodosa risk factors

A

hep B, C, older age, male

276
Q

polyarteritis nodosa - alternative to tissue biopsy

A

mesenteric or renal arteriography emonstrating multiple aneurysms and irregular constrictions

277
Q

polyarteritis nodosa =

A

vasculitis of medium sized muscular arteries

segmental transmural inflamm leads to fibrinoid necrosis

278
Q

polyarteritisi nodosa, rule out

A

ANCA

279
Q

polyarteritis nodosa presentation

A

systemic symptoms

multisystem organ damage

280
Q

polyarteritis nodosa - organ most commonly involved

A

kidney

281
Q

PAN transmural inflamm leads to

A

aneurysm of arterial wall

282
Q

PAN labs

A

increase WBC, ESR
decreased hgb, hct
proteinuria, hematuria

283
Q

polyarteritis nodosa - body parts affected

A

kidneys, heart, gi tract

muscle, nerves, joints

284
Q

PAN treatment

A

steroids

cyclophosphamide

285
Q

PAN skin manifestations

A

erythema nodosum like

palpable purpura similar to HSP

286
Q

PAN gi symptoms

A

ischemic abd pain (after meals, leads to wt loss)

287
Q

PAN CNS symptoms

A

named nerve s- both motor and sensory deficits

288
Q

PAN diagnosis

A

biopsy of tissue

289
Q

HSP pathophysiology

A

small vessel vascuilitis characterized by IgA

290
Q

HSP joint manifestations

A

transient non-migratory arthralgia

291
Q

HSP renal

A

iga immune complex deposition

292
Q

HSP treatment

A

mainly self limiting/supportive

otherwise, prednisone and acei and diuretics

293
Q

HSP GI symptoms

A

colicky abd pain

increased risk of intussusception

294
Q

HSP urinalysis

A

blood and protein in ruine

rBC casts

295
Q

HSP tetrad

A

palpable purpura
polyarticular arthritis
abd pain
renal failure

Internal Med (23 decks)

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