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Step Numero Uno > Quick and Dirty > Flashcards

Quick and Dirty Flashcards

1
Q

Pancoast tumor

A
  • Apex of lung tumor near SUPERIOR SULCUS - Non-small cell lung cancer (ie squamous or adeno) - Can compress and invade brachial plexus –> ipsilateral shoulder pain, upper limb paresthesias, & areflexic arm weakness - Involvement of cervical SYMPATHETIC ganglia –> Horner’s syndrome (partial ptosis, miosis, anhydrosis)
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2
Q

Ipsilateral shoulder pain upper limb paresthesia on ipsilateral side ptosis, miosis, anhydrosis on ipsilateral side

A

Pancoast tumor

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3
Q

On LM neurons w/ shrunken nuclei, no detectable nissl substance and intensely eosinophilic cytoplasm =?

A

IRREVERSIBLE cell injury –> red neuron (may also see pyknosis - condensation of chromatin)

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4
Q

Irreversible cell injury/Acute neuronal injury (red neuron)

A

-Shrunken nuclei - Loss of Nissl substance -Eosinophilic cytoplasm - Pyknosis of nucleus Visible 12-24 hours after injury

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5
Q

Axonal reaction due to loss of axon (type of response due to type of injury)

A
  • Enlargement of the cell body - Eccentric nucleus (moves to periphery) - Enlargement of the nucleolus - Dispersion of the Nissl substance
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6
Q

tumor near the superior sulcus

A

pancoast tumor (non-small cell lung cancer)

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7
Q

how long does it take to deplete folate stores?

A

Months in a normal individual, weeks in an alcoholic

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8
Q

How long does it take to deplete cobalamin stores?

A

Years

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9
Q

Pancytopenia, impaired blood cell differentiation, and clonal expansion of mutated hematopoietic cells in bone marrow with elevated MCV?

A

Myelodysplasia (premalignant condition)

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10
Q

What are signs of myelodysplasia?

A

Myelodysplasia is a premalignant condition that manifests w/: - Pancytopenia - Impaired blood cell differentiation - Clonal expansion of mutated hematopoietic cells in the bone marrow - Elevated MCV

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11
Q

Peripheral blood smear w/ folate deficiency will show what?

A
  • Macrocytosis (MCV > 100) - Ovalocytosis - Neutrophils w/ hypersegmented nuclei (>5)
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12
Q

Definition of sensitivity + formula

A

The probability of a diseased person testing positive [Of all the diseased, likelihood that this a TP] Sensitivity = TP/(TP+FN) (vertical on grid)

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13
Q

Definition of specificity + formula

A

The probability of a non-diseased person testing negative [Of all of the non-diseased, likelihood that this is TN] Specificity = TN/(TN+FP) (vertical on grid)

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14
Q

Definition of Positive predictive value + Formula

A

The probability that disease is present given a positive result [Of all the positives, the likelihood that this is a diseased (TP)] PPV = TP/(TP+FP) (horizontal on grid; effected by prevalence)

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15
Q

Definition of Negative Predictive value + formula

A

The probability that disease is absent given a negative result [Of all negatives, the likelihood that this is a non-diseased (TN)] NPV = TN/(TN+FN) (horizontal on grid; effected by prevalence)

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16
Q

Positive likelihood ratio definition + formula

A

Positive likelihood ratio = a ratio representing the likelihood of having the disease given a positive result LR+ = Sensitivity / (1 - Specificity)

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17
Q

Negative likelihood ratio definition + formula

A

A ratio representing the likelihood of having the disease given a negative result LR- = (1-Sensitivity) / Specificity

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18
Q

Are likelihood ratios affected by prevalence?

A

No

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19
Q

What does a likelihood ratio >1 or

A

Likelihood ratio >1 indicates that the respective test result is associated w/ the presence of the disease Likelihood Ratio

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20
Q

Low vitamin D levels causes what disease in children and what disease in adults?

A
  • Rickets in children - Osteomalacia in adults
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21
Q

What are the levels of serum Ca, phosphorous, and PTH found in an osteomalacia patient w/ deficiency of Vit D?

A
  • Serum Ca: low - Serum Phosphorous: low - Serum PTH: high (bc trying to fix low Ca levels –> inc bone resorption (–> osteomalacia) & inc. excretion of phosphorous)
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22
Q

Elevated PTH, hypERcalcemia, & hypOphosphatemia is found when?

A

Patients w/ primary hypERparathyroidism

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23
Q

Decreased serum PTH, decreased serum Ca, & inc. serum phosphorous?

A

HypOparathyroidism - can be caused by severe hypOmagnesemia which can be seen w/ prolonged diarrhea

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24
Q

HypOmagesemia esp w. prolonged diarrhea can cause what disease?

A

HypOparathyroidism (dec. serum PTH & Ca & inc. serum phosphorous)

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25
Q

What causes pseudohypoparathyroidism?

A

resistance to PTH (–> normal to low Ca, elevated phosphorous, elevated PTH)

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26
Q

Which ocular motor nerve (III, IV, VI) is most often affected by diabetes?

A

CNIII (oculomotor n.) - unilaterally

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27
Q

Symptoms of diabetic CN III mononeuropathy

A
  • acute onset diplopia - down and out position of eye - ptosis
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28
Q

Acute onset diplopia, down and out gaze, ptosis in a diabetic, what disease is most likely and what is the most likely cause?

A

Diabetic CN III mononeuropathy caused by ischemic nerve damage, predominantly involving the core of the nerve and sparing the peripheral part

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29
Q

The somatic component of CN III is located where in the nerve?

A

Centrally

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30
Q

The autonomic component of CN III is located where and what is it responsible for?

A

Peripherally located Responsible for pupillary constriction & accomodation

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31
Q

CN III mononeuropathy due to ischemic nerve damage predominantly involve what portion of the nerve & what would remain intact?

A
  • Predominantly involves the core of the CN III w/ relative sparing of the peripheral part - Pupillary size & reactivity is normal (b/c periphery where autonomic component is located is spared)
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32
Q

How can you tell the difference b/t CN III neuropathy due to ischemic nerve damage vs nerve compression?

A

Nerve compression damages periphery of nerve –> autonomic (parasympathetic) changes –> pupillary dysfunction (dilated pupil & loss of accomodation) Ischemic damage occurs in center of nerve –> motor changes w/ normal pupillary response –> acute onset diplopia, down and out gaze, ptosis

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33
Q

Causes of CN II nerve compression

A
  • Transtentorial (uncal) herniation - Neoplasms - Aneurysms of posterior cerebral & posterior communicating arteries
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34
Q

Midbrain lesions cause bilateral or unilateral ptosis?

A

MIdbrain lesions cause bilateral ptosis because bother levator palpebrae are innervated by a single subnucleus

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35
Q

Movement disorder with behavioral abnormalities such as aggressiveness, apathy or depression & dementia

A

Huntington Disease

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36
Q

Triad of Huntington disease

A
  • Chorea (movement disorder) - Behavioral abnormalities (aggressiveness, apathy, depression) - Dementia
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37
Q

Huntington disease has what kind of inheritance and penetrance?

A

Autosomal dominant w/ 100% penetrance (complete penetrance)

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38
Q

Which Huntington patients will will develop the disease earlier in life and why?

A

Huntington patients who receive the abnormal gene from their fathers b/c during spermatogenesis, CAG repeats rapidly increase while the number of trinucleotide repeats remains the same during maternal transmission.

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39
Q

Which diseases are commonly associated with anticipation?

A

Trinucleotide repeat disorders such as: - Huntington Disease - Fragile X Syndrome - Myotonic Dystrophy - Friedreich Ataxia

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40
Q

What is pleiotropy?

A

When one gene mutation leads to multiple phenotypic abnormalities. Is seen in Huntington’s b/c one gene mutation –> dysfunction in behavior, movement, and cognition

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41
Q

One gene mutation that leads to multiple phenotypic abnormalities

A

Pleiotropy

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42
Q

The presence of two populations of cells w/ different genotypes in one patient

A

Mosaicism Can be seen in Turner syndrome (46XX/45XO genotype), Klinefelter (46XY/47XXY) and Down Syndrome

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43
Q

Mosaicism is?

A

The presence of two populations of cells w/ different genotypes in 1 patient. Seen in Turner syndrome (46XX/45XO), Klinefelter (46XY/47XXY) and Down Syndrome

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44
Q

Jerky movements and happy disposition

A

Angelman syndrome, genomic imprinting –> inactivation of mother’s chromosome 15

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45
Q

Angelman syndrome

A
  • Inactivation of mother’s chromosome 15 (Genetic imprinting) - Jerky movements & happy disposition (“happy puppet”)
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46
Q

Prader-Willi syndrome

A
  • Inactivation of paternal chromosome 15 (genetic imprinting) - Insatiable hunger & thirst - Emotional lability (big swings)
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47
Q

Insatiably hungry & thirsty and emotionally unstable

A

Prader-Willi syndrome genomic imprinting –> inactivation of paternal chromosome 15

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48
Q

Granulosa-thea cell tumors are primarily identified in what population?

A

Postmenopausal women

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49
Q

Granulosa theca cell tumors are categorized as what type of tumor?

A

sex cord stromal tumors (derived from ovarian stroma)

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50
Q

The yellow coloration of an ovarian mass indicates what?

A

Lipid content and therefore hormonal activity

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51
Q

Granulosa-theca cell tumor’s composition is what?

A

Largely granulosa cells and a scattering of theca cells

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52
Q

A granulosa tumor is usually bilateral or unilateral?

A

Unilateral

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53
Q

Granulosa-theca cell tumors have what type of effect since they secrete what?

A

Feminizing effect b/c they secrete estrogen

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54
Q

Large amounts of estrogen release may cause what in prepubertal girls and in older women?

A

Girls – precocious sexual development Older women - fibrocystic change of the breast, endometrial hyperplasia, endometrial carcionma

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55
Q

Granulosa cells look like what histologically?

A

small, cuboidal cells that grow in cords or sheets.

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56
Q

What may be found in granulosa cell tumors that are small gland-like structures that contain acidophilic material?

A

Call-Exner bodies

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57
Q

Call-Exner bodies are found when and what do they look like?

A
  • Found in Granulosa cell tumors - Small, gland-like structures tat contain an acidophilic material - Suggestive of immature follicles
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58
Q

How do thecomas present histiologically?

A

Cells present as clusters or sheets of cuboidal cells

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59
Q

Tumors consisting primarily of thecoma cells are generally benign or malignant?

A

Benign

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60
Q

What tumors can be ID’d by human chorionic gonadotropin?

A

Trophoblastic and other germ cell tumors including extra-gonadal tumors.

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61
Q

Germ cell tumors can be ID’d from what hormone?

A

Human chorionic gonadotropin

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62
Q

What produces alpha fetoprotein?

A

Fetal liver and yolk salk normally

Some cancers:

hepatocellular, nonseminomatous testicular or ovarian carcinomas

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63
Q

What is a tumor marker for nonseminomatous testicular carcinomas, ovarian, hepatocellular carcinoma?

A

Alpha-fetoprotein (AFP)

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64
Q

Is CA-125 used as a screening tool for ovarian cancer?

A

No it is not specific enough

It is best used as a way to monitor therapeutic response

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65
Q

What glycoprotein is best used to monitor therapeutic response of malignant ovarian cancers?

A

Cancer antigen 125 (CA-125)

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66
Q

What ovarian cancers have elevated amounts of CA-125 on their surface?

A

Malignant epithelial cells in serous, endometrioid, and clear cell carcinomas of the ovary

67
Q

Coomon medications for treatment of CHF

A
  • Digoxin
  • Beta-adrenergic blocers
  • ACE inhibitors
  • Potassium sparing diuretics
  • Loop diuretics
68
Q

Which K sparing diuretics are prefered in heart failure patients?

A

Spironolactone and eplerenone are preferred in patients w/ heart failure as they can also prevent the deleterious effects of aldosterone-induced cardiac remodelling

*they competitvely inhibit the aldosterone receptor

69
Q

Infant experiences lethargy, vomiting, and jaundice soon after birth. The infant is placed on a galactose-free formula and shows gradual improvement. What enzyme is likely deficient in the infant and what disease is this?

A

Classic galactosemia caused by impaired galactose-1-phosphate metabolism.

70
Q

Galactose 1 phophate is convereted to glucose 1 phosphate by what type of reaction?

A

Epimerization (changing the chirality of the molecule)

  • requires UDP-glucose & glactose-1-phosphate uridyl transfersase (GALT)
71
Q

What enzyme is needed in the epimerization of Galactose 1P to Glucose 1P?

A

Galactose-1-phosphate uridyl transferase (GALT)

72
Q

Clinical symptoms of classical galactosemia

A

vomiting, lethargy, and failure to thrive soon after breasfeeding is begun

73
Q

Vomiting, lethargy, and failure to thrive soon after breastfeeding is begun cause by?

A

Classic galactosemia with deficiency in galactose-1-phosphate uridyl transferase (GALT)

74
Q

Galactosemia can result in what?

A
  • Impaired liver function
  • Hyperchloremic metabolic acidosis
  • Aminoaciduria
75
Q

Untreated galactomsemia typically culminates in what and why?

A

Untreated –> irreversible eye and liver damage due to build up of galactitol

76
Q

Clinical features of Polycystic ovary syndrome

A
  • Androgen excess (hirsutism, acne, androgenic alopecia)
  • Ovarian dysfunction (menstural irregulariy, polycystic ovaries)
  • Insulin resistance (acanthosis nigricans, glucose intolerance/diabetes, metabolic syndrome)
  • Obesity
77
Q

Hirsuitism, menstrual irregulariy, glucose intolerance, obese — what am i?

A

Polycystic ovary syndrome

78
Q

Treatment for polycystic ovary syndrome

A

weight loss, combination hormonal contraceptives, metformin (if hypERglycemic/diabetic)

79
Q

Elevated androgen levels in a woman can cause what?

A

Polycystic ovary syndrome –> enlargement of multiple follicles in ovary rather than normal process where only one follicle becomes dominant

Can –> amenorrhea & infertility

80
Q

in polycystic ovary syndrome what hormones are elevated?

A

Androgens –> enlargement of mulitple ovarian follicles + other symptoms

Estrogen –> endometrail hyperplasia and increased risk of endometrial cancer

81
Q

physical exam of polycystic ovaries desmonstrates what?

A

bilateral enlargement & smooth thickened capsuls

cut section –> subcapsular follicles in diff stages of atresia & hyperplastic theca stromal cells rim the arrested follicles

82
Q

Lesch-Nyhan syndrome is what type of inheritance?

A

X-linked recessive

83
Q

Lesch-nyhan syndrome caused by defect in what?

A

hypoxanthine-guanine phosphoribosyltransferase (HGPRT)

84
Q

defect in hypoxanthine-guanine phosphoribosyltransferase (HGPRT) is found in what disease?

A

Lesch-Nyhan syndrome

85
Q

Clinical features of Lesch Nyhan syndrome

A

self-mutilating behavior (finger/lip biting), mild mental retardation, involuntary movements, delayed motor development, nephrolithiasis and gout

Babies may have “frost” on the skin under the child’s diaper due to hyperuricuria (lots of urea in urine)

86
Q

Treatment of Lesch Nyhan

A

allpurinol to decrease uric acid levels

But no treatment for neurological symptoms

87
Q

Hypoxanthine guanine phosphoribosyltransferase does what?

A

Acts in purine salvage pathway

Catalyzes conversion of hypoxanthine & guanine to inosine monophosphate (IMP) and guanosine monophosphate (GMP)

W/o –> dec purine salvage, inc purine synth, hypERuricemia & hypER uricuria

88
Q

SCID caused by what enzyme deficiency

A

Adenosine deaminase (ADA)

89
Q

Deficiency of adenosine deaminase causes what?

A

SCID

90
Q

SCID is inherited how?

A

SCID is autosomal recessive

91
Q

What happens w/ a deficiency of adenosine deaminase?

A

Normally participates in purine catabolism, absence –> high conc. of dATP ==> inhib of ribonucleotide reductase –> inhib of DNA synth –> cell death

92
Q

What type of regulatory protein is able to dictate differntiation of a progeintor cell into a dermal cell?

A

Transcription factors

TFs are specific for each individual tissue and allow only those genes relevant to a the desired cell’s specific type to function and be expressed (so progenitor becomes a specific tissue)`

93
Q

Growth factors are:

A

proteins that stimulate the growth and differentiation of various cell lines, usually by regulating synth of transcription factors (ie GM-CSF or PDGF)

94
Q

controls what genes are expressed in order for a cell to differentiate properly

A

Transcription factor

95
Q

protein that stimulates growth and differentiation of various cell lines by regulating synth of transcription factors

A

Growth factors

96
Q

diverse group of proteins used in cellular signaling and intercellular communication

A

cytokines

97
Q

growth factors are one type of these diverse proteins

A

cytokines

98
Q

if we want a denervated eye’s pupil to constrict what kind of drug do we need?

A

A DIRECT cholinergic muscarinic AGONIST

  • must be direct b/c w/o innervation (meaning no nerve to release ACh) need a drug that works directly on the M3 receptors itself (w/o nerve help, bc indirect would inhib ACE but w/o nerves releasing ACh doesn’t matter)
99
Q

direct muscarinic cholinergic agonists such as what can cause pipillary constriction in the denervated eye?

A

Pilocarpine

100
Q

Person w/ pernicious anemia will likely overproduce what?

A

Gastrin

This is bc the immune-mediated destruction of gastric mucosa –> loss of parietal cells –> loss of HCl (& IF causing the pernicious anemia) –> nothing to inhib gastrin secretion (normally inhibited by hydrochloric acid)

101
Q

Pernicious anemia associated w/?

A

hypOchlorhydria & inc. serum gastrin levels

102
Q

What happens to a varicocele when lying down?

A

It dec in size or disappears as much of the blood returns to circulation

103
Q

acanthosis nigracans can be seen when?

A
  • Insulin resistance
  • Obesity
  • Malignancy (esp gastric or lung)
104
Q

The liklihood of malignancy inc w/ acanthosis nigricans when what happens?

A

It appears suddenly, spreads quickly, or involves the mucous membranes or palms and soles

105
Q

Name a vitamin K antagonist

A

WARFARIN!

106
Q

warfarin antagonizes what?

A

gama-carboxylation of vitamin K dependent clotting factors

107
Q

When are Glycoprotein IIb/IIIa inhibitors used?

A

In patients w/ acute coronary syndrome

108
Q

Are thromboolytics such as tpa used to prevent clot formation?

A

NO

they break down already existing fibrin clots

109
Q

Back pain unrelieved by rest in a pt w/ a firm prostatic nodule is strongly suggestive of what?

A

Prostatic cancer w/ the back pain signaling the presence of metastatic osteoblastic lesions in the vertebrae

110
Q

leuprolide acts like what when given in a pusatile manner vs continously

A

pulsatile –> GnRH analog

Continuously –> antagonist of GnRH –> long-term reduction of circulating gonadotropins (ie testosterone by dec ant pit release of LH; good for prostate cancer treatement)

111
Q

A patient w/ diGeorge syndrome likely has what cardiac structure malformed in utero?

A

Persitant Truncus arteriosus = a signle great vessel arises from the heart w/ aorta, pulm a. and coronary a. branching off from the ascending sement of this vessel

Normally truncus arteriosus divides in utero –> aorta & pulm a.

other conotruncal (outflow) tract defects include: tetralogy of fallort and interrupted aortic arch

112
Q

DNA methylation = ?

A

Enzymatic addition of methyl groups to cytosine residues in the genome –> effectively silences these genes (low transcriptional activity)

113
Q

What is the most common lysosomal storage disease?

A
114
Q

glucocerebroside deoposition in lysosome of macrophages is found in what disease?

A

Gaucher disease

115
Q

Gaucher cells are what and found in what disease?

A

Gaucher cells are macrophages filled w/ lipid glucocerebroside and look like filled w/ wrinkled tissue paper found in bone marrow.

Found in gaucher disease (lysosomal storage disease; most common)

116
Q

clinical findings of gaucher disease

A

hepatosplenomegaly, anemia, thrombocytopenia, bleeding, osteopenia, bone pain, and bone fractures

117
Q

clinical signs of tay-sachs

A

weakness, loss of motor skilss & cherry-red macula

118
Q

clinical manifestation of fabry disease

A

appear in childhood w/ severe extremity pain, dec ability to sweat, corneal & lenticular changes, GI dysfunction and angiokeratomas

119
Q

Which lysosomal storage diesases are x linked recessive?

A

Fabry’s and Hunter’s (hunters aim for the X)

all the rest are autosomal recessive

120
Q

niemann-pick symtoms

A

prodound abnormal neurologic function as toddler death by 2-3 yo

121
Q

metachromatic leukodystrophy symptoms

A

peripheral neuropathy & motor skills difficulties

death in early adulthood

122
Q

which 2 lysosomal storage diseases have lipid laden macrophages?

A
  1. Gaucher disease = has gaucher cells that look like tissue paper
  2. Niemann-Pick
123
Q

Gq proteins act on what?

A

Phopholipase C

124
Q

Where is IP3 found and what does it do?

A

Found in cyto and stimulated endoplasmic reticulum to release Ca –> smooth muscle contraction

125
Q

where is DAG fround and what does it do?

A

DAG is membrane bound and activates protein kinase C which will phosphorylate downstream messangers

126
Q
A
127
Q

Phopholipase C activates what?

A
  1. DAG
  2. IP3
128
Q

Which G protein activates DAG and IP3?

A

Gq by activating Phospholipase C –> activates DAG & IP3

129
Q

a1 causes smooth muscle vasoconstriction by what mechanism?

A

bind to receptor –> activate Gq –> activate Phospholipase C –> activate IP3 –> inc Ca release –> smooth muscle contraction

Note: phospholipase C also activates DAG

130
Q

anti TNF agents are?

A
  1. infliximab = monoclonal antibody to TNF-a
  2. etanercept = recombinant TNF receptor fusion protein
131
Q

stable angina = ?

A

chest pain that develops w/ exertion and resolves w/in 1-2 min of rest

132
Q

chest pain that develops w/ exertion and resolves w/in 1-2 min of rest =?

A

stable angina (ie angina pectoris)

133
Q

stable angina can prgress to acture coronary syndrome (ie unstale angina or MI) which is caused by what?

A

occlusion of coronary vasculature typically by a thrombus

134
Q

aspirin is useful at preventing clots by what mechanism?

A

NSAIDs are non-specific irreversible COX inhibitors (so btoh COX 1 & 2)

COX1 inhibition in platelets –> dec synth of thromboxane A2 (which is a potent stimulator of platelet aggregation and vasoconstriction)

NOTE: COX2 not present w/in platelets so not useful to inhib (but can’t help). It is actually helpful to keep around bc it produces prostacyclin (PGI2) which is an endothelial vasodilator

135
Q

focal segmental glomerulosclerosis is commonly scene in what settings?

A
  • HIV (HIV associated nephropathy
  • heroin addiction
  • sickle cell disease
136
Q

what is a poor prognosis variant of focal segmental glomerulosclerosis associated w/ HIV?

A

Collapsing glomerulopathy = the usual FSGS lesions + collapse & sclerosis of the whole glomerular tuft –> glomerular epithelial cells proliferate & hypertrophy + marked tubular injury w/ microcyst formation.

137
Q

Mutation of what gene is found in hand-foot genital syndrome?

A

Homeobox gene (ie HoxA-13)

138
Q

What are clinical conditions found in hand-foot-genital syndrome?

A
  • Clinodactyly (a finger or toe curving in)
  • Shortened thumbs & great toes (may make them severely hypOplastic)
  • Small feet
  • Urinary tract abnormalities
  • Genitourinary abnormalities (ie duplications of reproductive tract or bicornate uterus in women or hypOspadies in men)
139
Q

What does homeobox genes do?

A

They modulate expression of other genes in the cell –> guide dev from earliest stages of embryogenesis to final differentiation of cells

140
Q

Pax-3 mutations associated w/ what disease?

A

Waardenburg syndrome

  • heterochromia irides (different color eyes, 2 colors in same eye, or bright blue)
  • poliosis (white forelock; think Rogue)
  • dystopia canthorum (lateral displacement where the eyelids meet on side)
  • deafness
141
Q

what is erbB2?

A

It is an epidermal growth factor receptor that is overexpressed in breast cancer

142
Q

nephrogenic diabetes insipidus is caused by what?

A

vasopressin resistance in the renal collecting ducts

143
Q

nephrogenic diabetes inspidus has an increased what?

A

inc ADH level, renin, & aldosterone in an effort to inc water retention

also SERUM osmolality would inc (bc not retaining enough water)

NOTE: caused by ADH resistance in renal collecting ducts

144
Q

ADH resistance in renal collecting ducts =?

A

Nephrogenic diabetes insipidus

145
Q

Following a water deprivation test what would happen to a nephrogenic diabetes insipidus pt (serum & urine osmolarity, ADH level, renin level, and aldosterone level)?

A
  • Inc serum osmolality
  • Dec urine osmolality
  • Inc ADH level
  • Inc aldosterone
  • Inc renin
146
Q

Presence of GLUT-4 does what?

A

inc rate of muscle glycogen synth and glucose oxidation

147
Q

Sudden onset flank pain, gross hematuria, oliguria in a pt w/ high anion gap metabolic acidosis is suggestive of what?

A

Ethylene glycol poisoning

148
Q

ethylene glycol poisoning can cause obstruction bc?

A

ethylene glycol is metabolized to glycolate which is further metabolized to oxalate –> precipitates in kidneys –> calcium oxalate crystals (envelope) that cause tubular obstruction –> oliguria + flank pain

149
Q

MUDPILES

A
  • Methanol
  • Uremia
  • Diabetic Ketoacidosis
  • Propylene glycol/paraldehyde
  • Isoniazid/Iron
  • Lactic acidosis
  • Ethylene glycol (antifreeze)
  • Salicylates (aspirin)
150
Q

Infarction of middle cerebral artery can cause what visual abnormality?

A

Homonymous hemianopsia

infarct can damage the optic radiations

151
Q

sarcomere =?

A

distance from 1 Z line to the next Z line

152
Q

What is typically the darkest line on electron micrographs of muscle?

A

Z line

153
Q

What anchors at the Z line?

A

Thin filaments composed of actin, tropomyosin, and troponin

154
Q

I band consists of what?

Can it change size or remains the same?

A

I band contains Z line and the sections of thin filament anchored w/o overlapping w/ thick

It can change width depending upon contractile state

155
Q

What two items overlie the Z line and I band?

A
  1. Transverse tubules (tubules in communication w/ extracellular space)
  2. Terminal cisternae (extensions of the sarcoplasmic reticulum)
156
Q

M line =?

A

M line anchors the thick myosin filaments at center of sarcomere

157
Q

H band=?

A

Only the section of the sarcomere containing mysoin thick filaments that do not overlap w/ actin thin filaments (anchored to M line)

158
Q

A band = ?

A

All of the thick myosin filament even that which overlaps w/ thin actin filaments (anchored to M line)

159
Q

which parts of the sarcomere can change width?

A

H and I band

160
Q

Which part of the sarcomere has overlapping segments?

A

A band

161
Q

symptoms of pancytopenia

A
  1. anemia = fatigue
  2. leukopenia = opportunistic infx
  3. thrombocytopenia = bleeding complications

This is seen w/ leukemia (among other stuff)

162
Q

basophilic stippling seen in?

A
  • thalassemias
  • alcohol abuse
  • lead poisoning
163
Q

what is a prominent feature of aspergillus infx that facilitates disease progression?

A

Vascular invasion

aspergillus disseminates to distant organs via hematogenous spread

164
Q

portal hypertention resulting from alcoholic liver disease can cause splenomegaly through what mechanism?

A

Portal hypertension –> congestive hypersplenism –> back up of blood in spleen –> expansion of the red pulp (composed of blood filled sinuses)

Step Numero Uno (4 decks)

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