UW Deck 2 Flashcards

1
Q

runs through ventral pons

A

fibers of CNs 5-8, corticospinal tracts, medial lemniscus, lateral spinalothalamic tract

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2
Q

vagus by the ear

A

auricular branch: cutaneous sensation of posterior external auditory canal; stimulation of vagal nerve with otoscope speculum –> decrease HR and BP –> vasovagal syncope event

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3
Q

sensation to most of external auditory canal

A

trigeminal nerve

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4
Q

facial nerve PANS efferent

A

salivation: submandibular and sublingual

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5
Q

viral myocarditis histology

A

lymphocyte infiltrate, focal necrosis

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6
Q

heart failure + recent viral infxn

A

dilated cardiomyopathy due to viral myocarditis (virus damages heart) –> systolic dysfunction

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7
Q

LVH, concentric hypertrophy

A

diastolic dysfunction –> wall stress –> heart failure/systolic dysfunction

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8
Q

dilated cardiomyopathy

A

dx of exclusion (pericardial dz, CAD, valvular dz, congenital dz, cardiac rhythm disturbances), systolic dysfunction, decreased stroke volumes, increased end volumes, regurgitation, dilation of all 4 chambers, primary (idiopathic), secondary (exogenous toxic agents)

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9
Q

vasopressin increases reabsorption of

A

water and urea @ inner medullary collecting duct, V2-receptor mediated

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10
Q

kidney filtration

A

simple diffusion depending on starling forces; filtration coefficient (kf) depends on area of capillary available for diffusion and permeability of capillary membrane; net filtration pressure (use oncotic and hydrostatic pressure – don’t need coefficient)

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11
Q

calcium handling in kidney

A

50-60% filtered ca reabsorbed in proximal tubules (paracellular pathway), reabsorption by distal tubule depends on parathyroid hormone

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12
Q

creatinine

A

freely filtered, secreted a litle by proximal tubules

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13
Q

PAH

A

freely filtered, entirely secreted by proximal tubules

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14
Q

wolff-parkinson-white

A

accessory AV conduction pathway: conduction reaches ventricles via accessory pathway slightly faster than AV nodal pathway –> recurrent paroxysmal supraventricular tachycardia, ventricular preexcitation, shortened PR interval, delta wave at start of QRS, widened QRS. Can also set up reentry arrhythmia (down AV node, up accessory pathway, normal QRS)

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15
Q

ST segment

A

plateau phase

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16
Q

T wave

A

ventricular repolarization

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17
Q

viral meningitis (vs. bacterial)

A

lymphocytic predominance, slightly elevated CSF protein, no organism on CSF gram stain and culture, more moderate symptoms (no stupor, coma, severe meningeal irritation)

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18
Q

bacterial meningitis (vs. viral)

A

high protein, low glucose, neutrophils predominate, really high WBC, often positive CSF culture/gram stain; mental status changes, seizures

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19
Q

meningitis common sx

A

fever, headache, nuchal rigidity, photophobia, painful extraocular movements

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20
Q

aseptic meningitis bugs

A

MCC: enterovirus family: coxsachie, poliovirus, echovirus, enterovirus; enterovirus = fecal-oral transmission, don’t cause gastroenteritis

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21
Q

adult bacterial meningitis bugs

A
  1. s pneumo, 2. n meningitis
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22
Q

polio virus

A

fever, malaise, aseptic meningitis –> myalgia, asymmetric paralysis (legs), damages anterior horn LMN –> hyporeflexic

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23
Q

aseptic meningitis via respiratory droplets

A

varicella, mumps, adenovirus, these 3 can also cause encephalitis

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24
Q

sexually transmitted viruses that can cause aseptic meningitis

A

HIV and HSV 2 more common than HSV 1, EBV, and CMV

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25
Q

arboviruses that can cause aseptic meningitis

A

togaviridae, flaviviridae, bunyaviridae; most common in summer and fall when arthropods are most active

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26
Q

meningitis in HIV/AIDS

A

cryptococcus neoformans

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27
Q

cryptococcal meningitis

A

headache/fever/lethargy, immune compromised (cancers), low glucose, increased protein, lymphocytes predominate, increased cell count; transparent capsule on india ink stain of CSF (ink stains background, bug stays transparent), thick polysaccharide capsule

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28
Q

listeria meningitis

A

ampicillin, GP rod, tumbling motility

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29
Q

fungal cell wall

A

not made of peptidoglycan

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30
Q

increased mixed venous blood oxygen

A

abnormal hb (binds with greater affinity to oxygen), oxidative metabolism inhibition (cyanide toxicity)

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31
Q

Obstructive lung disease

A

increase PaCO2

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32
Q

Diffusion problem

A

calculate A-a gradient; more normal PaCO2 (because it diffuses 20x better than oxygen) decreased PaO2

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33
Q

Perfusion problem

A

CO2 and O2 do not equilibrate with outside

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34
Q

Calculate A-a gradient

A

arterial PO2 given by ABG; PAO2 @ sea level (alveolar gas equation) = 150 - (PaCO2/0.8)

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35
Q

normal A-a gradient

A

10-15 mmhg

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36
Q

normal PAO2 –> normal PaO2

A

104 mmhg –> 95-100 mmhg (below 95: hypoxemia); drop occurs due to bronchial venous blood

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37
Q

PO2

A

inspired air: 160 mmhg –> mixes with water in trachea: becomes 150 mmhg –> alveolus: 104 mmhg; venous blood equilibrates with alveoli (40 mmhg –> 104 mmhg) –> drops to 95-100 mmhg because of bronchial venous blood

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38
Q

PCO2

A

venous blood PCO2: 45 –> alveolar PCO2 = 40 –> trachea CO2: 0 mmHg

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39
Q

venous/alveolar equilibration

A

NL: full equilibration after passing through 1/3 of capillaries (fast diffusion, perfusion-limited equilibration); if capillary perfusion is poor: slower or incomplete equilibration; tracheal air = alveolar air; venous blood = arterial blood

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40
Q

poor ventilation, what would alveolar gas composition be?

A

close to venous gas composition

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41
Q

diffusion-limited gas exchange

A

emphysema, pulmonary fibrosis, exercise (high perfusion)

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42
Q

4 major causes of hypoxemia

A

right to left shunt (congenital heart diseases); V/Q mismatch (pneumonia, COPD, pulmonary embolism); alveolar hypoventilation (sedative overdose, sleep apnea, myasthenia gravis, high altitude –> low oxygen pressure in alveoli); diffusion problems (alveolar hyaline membrane disease)

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43
Q

cryptococcus neoformans

A

immunocompromised patients, inhaled –> asx lung infection/pulmonary cryptococcosis (mucicarmine stain lung tissue and bronchoalveolar washings) –> meningitis (india ink CSF); serologic testing (latex agglutination) to detect capsular antigen in CSF

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44
Q

oral thrush

A

white plaques, associated with immunosuppression, diabetes, antibiotics, steroids\

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45
Q

esophagitis

A

HIV+ candida infection, odynophagia, dx with endoscopy + bx

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46
Q

renal osteodystrophy

A

decreased calcitriol (active vitamin D), retention of phosphates (bind Ca –> exacerbates hypocalcemia) –> hyperparathyroidism + more bone turnover (exacerbates hyperphosphatemia)

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47
Q

hypercoagulable state

A

surgery

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48
Q

marantic endocarditis

A

disseminated cancer associated with hypercoagulability –> NBTE (non-bacterial thrombotic endocarditis)

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49
Q

non-bacterial thrombotic endocarditis (NBTE)

A

sterile fibrinous vegetations along edges of valves = thrombus, no inflammation, often due to hypercoagulable state due to underlying disease

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50
Q

trousseau’s sign

A

tumor-associated procoagulants release –> migratory thrombophlebitis (seen in pts with disseminated cancers)

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51
Q

hypercalcemia in hospitalized pt

A

hypercalcemia of malignancy, pth-like substance from tumor

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52
Q

extrahepatic biliary atresia

A

congenital, jaundice, dark urine/light stools, conjugated hyperbilirubinemia, intrahepatic bile ductular proliferation, portral tract edema and fibrosis, parenchymal cholestasis, increased alk phos, ggt

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53
Q

hemolytic disease in Rh+ newborn

A

jaundice, unconjugated hyperbilirubinemia, hemolytic anemia, + coombs test

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54
Q

gilbert dz

A

mild unconjugated hyperbilirubinemia during stress

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55
Q

A1AT deficiency, effect on liver

A

hepatic intracytoplasmic inclusions that are eosinophilic on H&E, strongly PAS positive

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56
Q

physiologic jaundice

A

goes away after a week

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57
Q

d-isoimmunization

A

Rh disease

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58
Q

most potent chemotactic eicosanoid

A

leukotriene B4 (also 5-HETE = leukotriene precursor)

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59
Q

irreversible changes in ASD

A

chronic pulmonary HTN –> permanent eisenmanger syndrome, pulmonary sclerosis so severe/irreversible that you can’t fix the ASD because the RV won’t be able to pump; atrial and ventricular enlargement can be reversed

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60
Q

long qt syndrome

A

if pt is otherwise healthy, long qt = congenital issue, predispose to torsades to points –> syncope or death; 2 common congenital disorders related to K+ channel mutation –> delayed rectifying K+ current

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61
Q

jervell and lange-nielsen

A

autosomal recessive, neurosensory deafness, long qts

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62
Q

romano-ward syndrome

A

more common than jervell and lange-nielsen, no deafness, long qt

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63
Q

sudden onset syncope

A

suggests arrhythmia

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64
Q

qt

A

start of qrs –> up to t wave

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65
Q

mutations that cause dilated cardiomyopathy

A

mutations that affect cytoskeleton proteins or mitochondrial enzymes

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66
Q

HOCM

A

syncope upon exertion

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67
Q

sarcoidosis

A

immune mediated = disordered immune regulation –> intraalveolar and interstitial accumulation of CD4 T cells –> high CD4/CD8 ratio in bronchoalveolar lavage fluid (differentiates sarcoidosis from hypersensitivity pneumonitis or AIDS-related lymphocytic interstitial pneumonitis - have low CD4/CD8 ratios)

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68
Q

high neutrophils in lungs

A

bacterial PNA, acute toxic injury

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69
Q

high CD8 cells in lungs

A

lung transplant + chronic rejection

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70
Q

intussusception

A

impaired venous drainage, necrosis, colicky abdominal pain, current jelly stools = mucus + blood

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71
Q

inferior mesenteric vein

A

does not course with the inferior mesenteric artery, drains into splenic vein –> portal vein

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72
Q

celiac trunk

A

supplies foregut except mouth, pharynx, proximal esophagus

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73
Q

internal iliac supplies certain parts of the gut

A

middle rectal artery, inferior rectal artery (via pudendal)

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74
Q

external iliac supplies

A

anterior abdominal wall, lower extremities

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75
Q

schwannoma tumor marker

A

S-100 (both melanomas and schwannomas are S-100 because both are derived from neural crest cells)

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76
Q

schwannoma etiology

A

can come from any CN (except 2) because they’re all covered by schwann cells, tumors of PNS

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77
Q

schwannoma histology

A

biphasic pattern (antoni a + b), spindle cells (elongated with regular oval nuclei), highly cellular areas = antoni a, low cellularity = antoni b, antoni a areas may have palisading patterns = picket fence)

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78
Q

mitral stenosis from acute rheumatic fever

A

takes years or decades to develop, MCC mitral stenosis = chronic rheumatic fever

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79
Q

myocarditis from ARF

A

can cause dilated cardiomyopathy –> mitral regurgitation

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80
Q

acute rheumatic fever and PSGN

A

rarely occur together, caused by different strains

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81
Q

ARF, sydenham

A

CNS involvement

82
Q

cirrhosis

A

diffuse hepatic fibrosis, normal lobular architecture –> nodular parenchymal regeneration, micronodular (<3 mm in diameter) or macronodular

83
Q

Dubin-Johnson

A

accumulation of course pigmented granules

84
Q

intrahepatic hydatid cysts + surrounding fibrosis

A

echinococcus

85
Q

granulomatous destruction of bile ducts

A

primary biliary cirrhosis

86
Q

hereditary pancreatitis

A

mutated trypsinogen that cannot be inactivated by pancreatic secretory trypsin inhibitor (PSTI) –> premature activation + recurrent acute pancreatitis

87
Q

gastric adenocarcinoma

A

associated strongly with h. pylori

88
Q

liver cirrhosis most commonly associated with

A

alcoholism, hep b and c

89
Q

megaloblastic anemia associated with

A

B12, folate deficiency, methotrexate, phenotoin, some inborn metabolic errors

90
Q

common colds

A

coronavirus, rhinovirus, adenovirus

91
Q

bronchopneumonia

A

patchy inflammation of a number of lobules

92
Q

interstitial pneumonia

A

inflammation confined to alveolar walls

93
Q

lobar pneumonia

A

inflammation involves entire lobe; 4 phases: congestion (first 24 hrs: vascular dilatation, alveolar exudate mostly bacteria, red/boggy lung) –> days 2-3: red hepatization: alveolar exudate contains erythrocytes, neutrophils, fibrin, red firm/hepatocyte-like –> days 4-6: gray hepatization: gray/brown firm lobe, RBCs disintegrated, fibrin and neutrophils remain –> resolution: enzymatic digestion of exudate

94
Q

diastolic depolarization

A

depolarization of SA, AV node occur during diastole

95
Q

crohn’s

A

increased Nf-kb –> increased cytokines and inflammation, but persistence of microbes –> chronic inflammation

96
Q

inflammatory bowel disease

A

multigenic, possibly involves HLA, NOD2 (intracellular microbe receptor –> triggers Nfkb)

97
Q

nfkb

A

responsible for cytokine production, connected to microbial recognition

98
Q

renal plasma flow

A

decreased by angiotensin 2, epinephrine, norepinephrine

99
Q

myxoma

A

constitutional symptoms (myxoma produces IL-6 –> fever, weight loss), mid-diastolic rumble over apex, positional CV sx (syncope, dyspnea)(valvular obstruction depends on position), embolic sx, large pedunculated mass on LA; histology = scattered cells within mucopolysaccharide stroma, abnormal blood vessels (myxoma produces a lot of vascular endothelial growth factor), hemorrhaging

100
Q

endocarditis

A

risk factors: prosthetic valves, valvular disease, IVDU, immunosuppression, vegetations seen on echo, typically a regurgitant murmur

101
Q

AML

A

pancytopenia (anemia, neutropenia, thrombocytopenia)

102
Q

light from optic tract –>

A

mainly lateral geniculate nucleus, also suprachiasmatic nucleus (circadian rhythms), pretectal areas (light reflex), superior colliculus (reflex gaze); from lateral geniculate nucleus –> optic radiations (meyer’s loop + baum’s loop) –> primary visual cortex

103
Q

damage to meyer’s loop

A

contralateral superior quadrantanopia

104
Q

temporal lobe lesions

A

aphasia (dominant hemisphere lesions), memory deficits, hallucinations (visual, sensory, auditory), seizures (complex partial and tonic-clonic)

105
Q

heart failure cells

A

pulmonary HTN –> RBCs extravasate into alveoli –> digested by macrophages, iron-containing macromolecules converted to hemosiderin –> hemosiderin-containing alveolar macrophages = heart failure cells = indicate pulmonary congestion/edema associated with heart failure

106
Q

golden or brown cytoplasmic granules

A

hemosiderin or lipofuscin, use Prussian blue stain to differentiate

107
Q

Prussian blue stain

A

detects intracellular iron (turns blue)

108
Q

pulmonary htn associated with congestion of pulmonary capillaries

A

only when HTN is distal to capillaries (LH failure); if proximal to capillaries, then capillary pressures are okay (ex: COPD, interstitial lung disease, pulmonary embolism, autoimmune vasculitis; airway obstruction –> pulmonary arterial hypertension)

109
Q

granulomas in lung tissue

A

TB, fungal infections, inhalation of foreign particles, beryllium, wegener’s, sarcoidosis, histiocytosis

110
Q

non-caseating granulomas in lung tissue - appearance

A

tightly clustered macrophages surrounded by rim of mononuclear cells, multinucleated giant cells

111
Q

barrett’s esophagus

A

intestinal columnar epithelium with goblet cells = should not be there (esophagus normally has stratified squamous epithelium), metaplasia adaptive at first but increases risk of adenocarcinoma; acid –> inflammation and necrosis of normal esophageal epithelium

112
Q

risks for squamous carcinoma of esophagus

A

alcohol, smoking, achalasia, nitrosamine-containing foods, plummer-vinson syndrome

113
Q

neurofibromas

A

short, sessile, or pedunculated cutaneous lesions, associated with NF-1 mutation (autosomal dominant), tumors of schwann cells (derived from neural crest), cutaneous and subcutaneous, rubbery texture

114
Q

Neurofibromatosis 1

A

cafe-au-lait spots (smooth or irregular borders), lisch nodules (pigmented hamartomas of iris = asx), optic gliomas (can cause blindness), other brain tumors (weakness, headaches, different sx)

115
Q

conus medullaris syndrome (damage to L2)

A

flaccid paralysis of bladder and rectum, impotence, and saddle anesthesia (S3-S5)

116
Q

cauda equina syndrome

A

cauda equina has 18 spinal/peripheral nerves: low back pain radiating to one or both legs, saddle anesthesia and loss of anocutaneous reflex (S2-S4, pudendal nerve), bowel and bladder dysfunction (S3-S5)

117
Q

T12

A

where lumbar spinal nerves originate

118
Q

achilles reflex

A

S1 and S2, tests integrity of sciatic nerve (S1 and S2 also do sensation of posterior leg and thigh)

119
Q

knee jerk reflex

A

L3 and L4 (part of femoral nerve)

120
Q

Wernicke korsakoff syndrome

A

if give dextrose infusion without thiamine to alcoholic/malnourished patient –> drop in thiamine concentration –> pyruvate DH needs thiamine –> brain can’t metabolize glucose –> necrosis of mammillary body

121
Q

thalamus

A

responsible for relaying information between spinal cord and cortex

122
Q

chronic thiamine deficiency

A

korsakoff psychosis

123
Q

Mammillary body

A

part of Papez circuit (part of limbic system, does emotion and memory)

124
Q

c-ANCA

A

antibodies against lysosomal enzymes in neutrophils and monocytes, found in Wegener’s = necrotizing granulomatous vasculitis

125
Q

Wegener’s

A

triad: pulmonary sx (necrotizing granulomas in the lung), upper respiratory tract (mucosal granulomas that ulcerate, sinusitis), renal dz (RPGN)

126
Q

RPGN associated with wegener’s

A

type 3 = pauci-immune, high c-ANCA in blood, no antibodies/complement/immune complexes found in the kidney (unlike goodpasture’s)

127
Q

IgA nephropathy

A

2-3 days after respiratory infection (much sooner than PSGN), also kids and young aduls (like PSGN)

128
Q

myxomatous degeneration/mitral valve prolapse

A

MC abnormality predisposing to native valve bacterial endocarditis in the US (not rheumatic fever anymore due to antibiotics); MVP predisposes to infected vegetations (fibrin collects on MVP, bugs collect on fibrin during periods of bacteremia) –> vegetations can throw thrombi

129
Q

native valve bacterial endocarditis

A

most commonly involves mitral valve (most common abnormality = MVP), predisposing factors: mitral regurgitation (in the US, MR used to be most frequently caused by rheumatic fever, now it’s most frequently caused by myxomatous degeneration)

130
Q

nonbacterial endocardial thrombus formation

A

high pressure against endocardial endothelium (mitral regurg: from high pressure to low pressure compartment)

131
Q

calcification of mitral annulus

A

most common in older people, hx of myxomatous degeneration or high ventricular pressures

132
Q

hemangioma

A

well-circumcised masses of spongy tissue; cavernous, blood filled vascular spaces of various sizes, lined by epithelial layer, mostly benign

133
Q

idiopathic membranous nephropathy

A

associated with IgG4 antibodies against phospholipase A2 receptor (only applies to idiopathic, not SLE membranous nephropathy)

134
Q

amyloidosis of kidney related to multiple myeloma

A

related to deposition of light chains

135
Q

systemic/multi organ amyloidosis in primary systemic amyloidosis

A

deposition of immune globulin light chains; primary systemic amyloidosis associated with monoclonal B cell proliferation (multiple myeloma)

136
Q

respiratory drive

A

respiratory rate set by medullary respiratory center, input from central and peripheral chemoreceptors; CO2 readily diffuses across blood-brain barrier, creates H+, activates medullary respiratory center

137
Q

respiratory drive in pt with COPD

A

chronic hypercapnea –> medullary respiratory center no longer responds to high levels of CO2, only drive to breathe is low O2 –> giving O2 is dangerous because it can eliminate their drive to breathe

138
Q

carotid sinus

A

internal carotid artery

139
Q

central chemoreceptors

A

indirectly sense arterial CO2, directly sense H+ (created by CO2 that has crossed the blood brain barrier)

140
Q

minimal change disease

A

immune mediated: responds to steroids, associated with infection; increase in anionically charged proteins (albumin)

141
Q

disruption of glomerular basement membrane

A

alport

142
Q

diabetic glomerulonephropathy

A

hyaline masses in mesangium, eosinophilic

143
Q

focal tubular necrosis and epithelial shedding

A

acute tubular necrosis, often accompanied with rupture of basement membranes

144
Q

heteroplasmy

A

mitochondria are distributed unevenly to daughter cells –> some cells have mostly NL or abNL mitochondria –> creates variety in disease expression

145
Q

mitochondrial encephalopathy

A

with lactic acidosis and stroke-like episodes

146
Q

variable expressivity

A

differences in phenotype of an autosomal dominant disorder

147
Q

complement-mediated cytotoxicity

A

IgG, IgM; IgM can effectively activate C1 because C1 needs to bind 2 or more antibodies (IgM = pentamer)

148
Q

anaphylaxis

A

systemic version of allergic reaction

149
Q

type 1 hypersensitivity MOA

A

first contact –> B cells undergo class switching to IgE –> IgE bind to IgE Fc receptors on basophils and mast cells –> second exposure –> cross-linking, degranulation, release of histamine, heparin, leukotrienes, others –> systemic vasodilation, increase in vascular permeability, bronchoconstriction –> hemodynamic and respiratory instability

150
Q

type 1 hypersensitivity clinical situations

A

asthma, anaphylaxis

151
Q

superior mesenteric artery

A

leaves aorta at L1; SMA syndrome: SMA and aorta trap/obstruct the transverse duodenum because of decreased angle between SMA and aorta (aortomesenteric angle decreases secondary to diminished mesenteric fat, pronounced lordosis, or surgical correction of scoliosis)

152
Q

transverse duodenum

A

courses horizontally at L3, between aorta (posterior) and SMA (anterior)

153
Q

renal arteries

A

originate from aorta at L1, IVC (formed by right and left common iliac veins at L4-L5) is anterior to right renal artery

154
Q

thoracic duct

A

empties into left subclavian

155
Q

anal fissure

A

fear in mucosa, majority occur at posterior midline of anal verge (distal to pectinate line, line between anal skin and perianal skin), posterior anal canal relatively poorly perfused (more sensitive); anal fissures associated with constipation; severe tearing pain; may have a skin tag

156
Q

obstructive PFT profile

A

decreased FEV1/FVC, increase in TLC and RV

157
Q

restrictive PFT profile

A

decreased TLC and FVC due to decreased lung expansion

158
Q

COPD clinical

A

progressive exertional dyspnea (emphysema), frequent respiratory infections (chronic bronchitis)

159
Q

heart failure

A

heart cannot pump enough blood, or it can only do so with elevated ventricular filling pressure

160
Q

diastolic heart failure pathophysiology

A

decreased ventricular relaxation/compliance, increased ventricular stiffness, caused by HTN/LVH and MI

161
Q

diastolic heart failure, pressure/volume curve

A

bottom curve moves up and to the left; EF remains the same, LVEDP increases to abnormally high in order to achieve near-normal LVEDV/stroke volume (always trying to normalize CO/BP)

162
Q

systolic dysfunction

A

decreased EF, reduced CO at normal LVEDV, increases to abnormally high LVEDV/LVEDP in order to increase CO (always try to normalize CO and BP during compensation)

163
Q

diastolic vs. systolic

A

diastolic only increases LVEDP (normal LVEDV, normal contractility), systolic failure increases LVEDP and LVEDV (abnormal contractility)

164
Q

enlargement of LA can compress

A

left recurrent laryngeal nerve (loops behind ligamentum arteriosum, underneath and around aortic arch, back up alonside trachea to the larynx = Ortner syndrome: neurapraxia –> left vocal cord paresis and hoarseness

165
Q

hoarseness

A

vocal cord disease or malfunction

166
Q

x-linked agammaglobulinemia

A

increased risk for streptococci and staphylococci; normal responses to listeria and viruses (intracellular), and fungi

167
Q

neonates up to 3 months

A

not yet fully developed cell-mediated immunity, at risk for listeria (rarely causes disease in normal healthy adult)

168
Q

candida

A

normal skin and mucous membrane flora; causes systemic illness in immunecompromised (opportunistic); skin and mucous infections if pt doesn’t have local pre-formed T cells (cutaneous candidiasis, oral thrush, esophageal candidiasis, vulvovaginitis); systemic infections if pt doesn’t have neutrophils (right-sided endocarditis, kidney and liver abscesses, candidemia); polymorphic (seen as budding yeast or pseudohyphae)

169
Q

deficiency in complement

A

SLE-like disease, neisseria gonorrhea, neisseria meningitis

170
Q

blastomyces dermatitidis

A

ohio and mississippi river valleys, great lakes region, pulmonary: PNA; disseminated: common and severe; bx: large round yeast and single broad based bud

171
Q

dimorphic fungi (molds with hyphae in RT/25-30, yeast in body temp 35-37)

A

blastomyces, coccidioides (paracoccidioides), spirothrix, histoplasma

172
Q

sporothrix schenkii

A

gardening/thorn prick, pustules, ulcers, subcutaneous nodules along lymphatics, culture: branching hyphae, bx: round or cigar-shaped budding yeast

173
Q

coccidioides immitis

A

southwestern states, mold form in soil, pulmonary form: flu-like illness, cough, erythema nodosum, disseminated form: affects skin, bones, lungs; bx: doubly refractile thick-walled spherules filled with endospores

174
Q

histoplasma capsulatum

A

ohio and mississippi river valleys, soil, bird, bat droppings; pulmonary: similar to tb (lung granulomas); disseminated: lungs, spleen, liver; bx: oval yeast cells within macrophages

175
Q

paracoccidiodes

A

central and south america, mucocutaneous or cutaneous ulcers, can progress to LNs/lungs, bx: cells covered in budding blastoconidia

176
Q

aspergillus

A

mold form only, septate hyphae with acute angles, mainly immunocompromised pts

177
Q

malassezia furfur

A

cutaneous mycosis (hypopigmented patches), KOH preparations of skin scrapings = short hyphae and spores = spaghetti and meatballs

178
Q

rhizopus, mucor, absidia

A

saprophytic fungi, causes mucormycosis in immunocompromised; mold form of rhizopus and mucor = nonseptate hyphae and wide angles, paranasal infxn in diabetic pts

179
Q

fungal sinus infections

A

aspergillus, mucor (mucor in diabetics and immunocompromised)

180
Q

hemochromatosis genetic mechanism

A

HFE mutation, abnormally high iron intestinal absorption, HFE expressed on basolateral side - binds transferrin and takes in iron –> amount of iron taken into the cell regulates cell’s uptake of iron from the gut

181
Q

hemochromatosis clinical presentation

A

affects heart, pancreas, liver - cirrhosis, HCC

182
Q

iron deficiency anemia

A

celiacs

183
Q

basal ganglia atrophy

A

wilson’s disease

184
Q

mycobacterial infections

A

require IFN-g; infected macrophages –> secrete IL-12 –> Th1 cells secrete IFN-g –> helps with phagocytosis; defects in this pathway –> disseminated mycobacterial infections, require lifelong antimycobacterial agents

185
Q

x-linked agammaglobulinemia

A

predisposed to lower respiratory infections and giardia

186
Q

s epidermidis

A

ubiquitous on skin, attaches to foreign objects in the body, synthesis biofilm (extracellular polysaccharide matrix) that protects bugs from antibiotics, opsonization, neutrophil migration, t-cell activation –> can then release bugs into the bloodstream –> must remove foreign object infected with biofilm; MCC of endocarditis with prosthetic valves and septic arthritis for joint replacement

187
Q

tx s epidermidis

A

should treat aggressively pending organism identification and antimicrobial susceptibility; initial empiric treatment with vancomycin +/- rifampin or gentamicin due to widespread antibiotic resistance of s. epidermidis (especially in nosocomial infxns)

188
Q

staphylococcal tx

A

ciprofloxacin resistance seems to accompany methicillin resistance; methicillin resistance likely means cephalosporin resistance bc methicillin resistance = alteration of penicillin binding protein (same protein bound by cephalosporin)

189
Q

obligate intracellular organisms

A

chlamydia, rickettsia

190
Q

facultative intracellular organisms

A

legionella, listeria, mycobacteria, salmonella, neisseria

191
Q

Staph aureus

A

most pathogenic staph (coagulase positive = able to clot blood); produces yellow pigment; endocarditis in IVDU; MCC osteomyelitis

192
Q

staph aureus protein A

A

cell wall component, binds Fc portion of IgG, prevents complement fixation and phagocytosis

193
Q

food poisoning by staph

A

staphylococcal enterotoxin

194
Q

enveloped viruses

A

susceptible to ethers and other organic solvents which dissolve the envelope –> lose infectivity

195
Q

viral heat stability

A

destroyed by heating 50-60degrees for 30 minutes

196
Q

death by diarrhea

A

MCC in 3rd world = viruses;

197
Q

staph vs. strep

A

staph = clusters; strep = chains

198
Q

catalase test

A

differentiates staph (positive) vs. strep (negative)

199
Q

neisseria meningitidis

A

GN kidney-bean shaped cocci; lipooligosaccharid (LOS) correlates with morbidity and mortality, outer membrane LOS acts like LPS of enteric GNRs, sepsis by inducing systemic inflammatory response, cutaneous petechiae/hemorrhagic bullae, lacks O-antigen of LPS, capsule helps resist phagocytosis but is not associated with morbidity/mortality, protective antibodies are directed against capsular polysaccharide (vaccine = capsule polysaccharides); URI, meningitis, meningococcemia

200
Q

lancet shaped

A

strep pneumo