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MSII Pathology > Unit 1 Lectures > Flashcards

Unit 1 Lectures Flashcards

1
Q

what is the most likely explanation for hyperthyroidism in pregnant women?

A

hCG is homologous to TSH (thyrotropin) and stimulates excess release of TH from thyroid gland

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2
Q

what is hyperemesis gravidarum?

A

intractable nausea, may be caused by extremely high hCG (also due to hyperthyroidism)

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3
Q

what is a complete VS incomplete/partial hydatidiform mole?

A

complete: empty ovum is fertilized with an X sperm that duplicated
- proliferates widely as a tumor, isntead of a normal fetus

incomplete: egg was fertilized by 2 sperm or 1 sperm that duplicated, so it becomes 69 or 92 Xm
- usually dies quickly

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4
Q

explain the gravida and para X-X-X-X system?

A

gravida = how many times one has been pregnant
para = full term - pre-term - abortion - living children
-Floriday Power and Light

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5
Q

what are the three MUST GIVES for OB-GYNs?

A
  1. betamethasone - improve outcomes for neonates that are delivered prematurely
    - intramuscular to decrease intra-cranial hemorrhage, necrotizing encephalitis
  2. zidovudine - prevent vertical transmission of HIV to baby
  3. progesterone supplementation
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6
Q

what is consumptive coagulopathy?

A

inability to clot following hemorrhage, because so many clotting factors have been used up
-can lead to DIC

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7
Q

what is Sheehan syndrome?

A

pan-pituitary dysfunction

  • susceptible to hypoperfusion in times of shock
  • usually anterior pituitary, but can be both
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8
Q

why is the GTT important to perform in PCOS women?

A

for every year a woman has PCOS, the risk for developing glucose intolerance and/or DMII rises
-GTT is most reliable test to rule out clinically significant glucose intolerance

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9
Q

what are myoepithelial cell markers (normally)?

A

calponin
smooth muscle myosin heavy chain
p53

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10
Q

what is a sclerosing adenosis?

A

lobulocentric proliferative lesion

  • mostly in association with fibrocystic change
  • may to detectable upon palpation and X-ray
  • usually <2 cm
  • often associated with calcifications
  • show 1.5 to 2-fold increase in breast cancer risk
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11
Q

what are details on fibroadenomas?

A

stromal cells express ER-beta, while epithelial cells variably express Er-alpha
-both express PR

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12
Q

what is adenomyoepithelioma of the breast?

A

uncommon benign lesion composed of proliferating epithelial and myoepithelial cells

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13
Q

explain what “triple negative” and “basal-like” means for breast cancer?

A

3-: it means it is negative for ER, PR (hormone receptors), and HER2/Neu (about 10-20% of breast cancers)

basal: tumors have cells with features similar to basal cells surrounding mammary (most have p53 mutations)
- most, but not all, triple-negative are basal-like (and vice versa)
- occur in younger and African-American women
- most BRCA1 tumors are both triple-negative and basal-like
- often aggressive with poor prognosis

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14
Q

what are stats on BRCA1/2 mutations?

A
  • increase risk of ovarian cancer from 2% up to 70%
  • reduce risk by having prophylactic oophorectomy
  • increased risk of pancreatic, prostate, colon, and second primary cancer
  • defective tumors have specific patterns of genetic alterations required for tumor genesis
  • 1:400 to 1:800 people have BRCA1/2 mutation
  • -1:40 Ashkenazi Jews
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15
Q

relationship between Myb, p53, and BRCA1 mutation?

A

Myb amplification and p53 mutation with different pattern frequently occur in BRCA1 deficient tumros compared to sporadic ones

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16
Q

what is beer potomania?

A

hyponatremia/kalemia due to excessive beer

-cause dizziness, muscle weakness, neurological impairment, seizures

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17
Q

is the osmotic force exerted by PRO and phosphates greater in intracellular space or extracellular space? what prevents them from swelling?

A

intracellular space

-Na/K ATPase prevent lysing

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18
Q

how is extracellular osmolality determined? how is this different from normal serum tonicity?

A

(Na+ x 2) + (Glu / 18) + (BUN / 2.8) + alcohol (usually 0) = usually 289

  • x2 takes Cl- into account
  • 18 is MW of glucose
  • 2.8 is MW of N2

NST doesn’t include BUN or alcohol (=285)

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19
Q

what are DDx for hypovolemia (low Na, low water)?

A

increased renal losses (high FENa)

  • aldosterone deficiency
  • glucocorticoid deficiency
  • Barrter’s/Gitelman’s syndrome
  • Fanconi’s syndrome
  • Diuretics (acutely)

Increasex extrarenal losses (low FENa)

  • GI losses
  • skin losses
  • hemorrhage
  • sepsis
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20
Q

what are DDx for euvolemia (unchanged Na, high water)?

A

low free water clearance (high Uosm)

  • SIADH
  • hypothyroidism
  • reset osmostat

high water intake (low Uosm)

  • primary/psychogenic polydipsia
  • beer potomania
  • “tea and toast”
  • hypokalemia
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21
Q

what are DDx for hypervolemia (high Na, higher water)

A 
renal issue (high FENa)
-renal failure

extrarenal issue (low FENa)

  • congestive heart failure
  • cirrhosis
  • nephrotic syndrome
  • severe hypothyroidism
22
Q

what can prevent acute kidney injury (AKI)?

A
  • volume expansion
  • allopurinol
  • rasburicase
  • dialysis
  • phosphate binder
23
Q

how can intracellular shifts of K+ into extracellular space cause hyperkalemia?

A
  • insulin deficiency (diabetes)
  • acidemia (usually metabolic)
  • cell lysis (TLS, rhabdomyolysis, hemolysis)
24
Q

how can decreased excretion from kidney cause hyperkalemia?

A
  • not filtered (AKI, CKD, ESRD)
  • insufficient Na+ delivery to distal tubule (pre-renal)
  • aldosterone issue (lack of production, resistance problem from medications or cell damage)
25
Q

what are three types of treatment of hyperkalemia?

A
  1. stabilizers (Ca++ only if EKG changes are noted)
  2. shifters (insulin+glucose, beta-2 agonist, sodium bicarbonate)
  3. removers (Kayexalate+sorbitol if colon working, kaliuretic or sodium bicarbonate if kidneys working, dialysis)
26
Q

treatment if hyperkalemia without EKG changes

A

K+ level is:
5-5.5 –> dietary restriction
5.5-6.5 –> above plus excretion enhancer
6.5-7 –> above plus compartmental shifters
>6.5 –> dialysis if above cannot help

27
Q

what are causes of anion gap acidosis?

A 
gain of non-HCl
exogenous
-methanol
-ethylene glycol
-ethyl alcohol
-isopropyl alcohol
-salicylic acid
-paraldehyde

endogenous

  • diabetic ketoacidosis
  • L-lactic acidosis (shock)
  • D-lactic acidosis (gut flora, small bowel loss)
  • uremia
28
Q

what are causes of hyperchloremic acidosis?

A 
loss of bicarbonate/gain of Cl
GI losses (diarrhea, ureteral-enteric diversions)
renal losses (renal tubular acidosis, excessive saline infusion)
29
Q

what tests can support carcinoid?

A

urine 5-HIAA

30
Q

PCOS patients have high serum levels of what hormones?

A

C-peptide
LH:FSH ratio
testosterone

NOT PRL

31
Q

what is an intestinal-type adenocarcinoma?

A

gastric adenocarcinoma

elevated mass with heaped up borders and central ulceration

32
Q

what is linitis plastica?

A

gastric adenocarcinoma

gastric wall is markedly thickened and regal folds are partially lost

33
Q

what is the “normal” number of antral follicles?

A

16-30

34
Q

what is normal male:

  • ejaculate volume
  • sperm concentration
  • motility
  • rapid progressive motility
  • normal morphology
A 
>1.5 mL
>15 million/mL
>40%
>32%
>4%
35
Q

what is the modified Ferrima-Gallwey Scale?

A

where hair would distribute in PCOS
Part 1: upper lip, chin, chest, anterior abdomen above umbilicus, genitalia to umbilicus
Part 2: upper arms/thighs/back/shoulder, lower back/buttocks

36
Q

what is a cold cone biopsy?

A

a large area of tissue around the cervix is excised for examination

37
Q

what are the stages for cervical cancer? 0 to IV and 5-year survival

A

0: carcinoma in-situ (100%)
I: confined to cervix (85%)
II: disease beyond cervix but not to pelvic wall or lower 1/3 of vagina (65%)
III: disease to pelvic wall or lower 1/3 vagina (35%)
IV: invades bladder, rectum, or metastasis (7%)

AKA FIGO staging

38
Q

explain Hodgkin’s staging (I - IV)

A

I: single lymph node region or single extralymphatic site (Ie)
II: 2+ sites, same side of diaphragm or contiguous extralymphatic site (IIe)
III: both sides of diaphragm or spleen (IIIs) or contiguous extralymphatic site (IIIe)
IV: diffuse involvement of extralymphatic sites +/- nodal disease

39
Q

what are major symptoms of Hodgkin’s lymphoma?

A
  1. unexplained weight loss > 10% in 6 mo
  2. fever
  3. night sweats
40
Q

diagnostic criteria for gestational hypertension

A

BP > 140/90

41
Q

diagnostic criteria for mild preeclampsia

A

BP > 140/90
proteinuria > 1+
protein:creatinine > 0.3
24h protein > 300 mg

42
Q

diagnostic criteria for severe preeclampsia

A 
BP > 160/110
proteinuria > 3+
24h protein > 5,000 mg
creatinine > 1.2 mg/dL
elevated transaminase
headache, visual changes, upper abdominal pain
oliguria, eclampsia, thrombocytopenia, pulmonary edema
fetal growth restriction
43
Q

explain the triad of preeclampsia

A
  1. vasoconstriction
  2. endothelial cell dysfunction/death
  3. tissue hypoxia

when the burden becomes clinically significant, the result is end-organ dysfunction
-as organs are affected, nature of end organ dysfunction becomes predictable

44
Q

what is HELLP?

A

syndrome of hemolysis, elevated liver enzymes, low platelets

45
Q

relationship between preeclampsia and kidney

A

glomerular endotheliosis

  • primary changes: swelling of damaged endothelial cells, leading to partial closure of many capillary lumens
  • mitosis within an endothelial cell is a sign of cellular repair
  • diffuse IgM deposition shows nonspecific entrapment of larger proteins in the more permeable glomerular capillary wall, instead of forming immune complexes
46
Q

what are brain and liver related complications of preeclampsia?

A
  • massive intraventricular hemorrhage

- hepatic infarction and necrosis

47
Q

preoperative evaluation of molar pregnancy

A
  • baseline quantitative hCG level
  • baseline chest XR to check for metastatic disease
  • complete blood count
  • blood type and Ab screen
  • clotting function studies (protime, partial thromboplastin time, fibrinogen)
  • thyroid function studies, preeclampsia, HELLP syndrome work up
48
Q

early signs of ovarian cancer

A
  1. increased abdominal girth or bloating, with pain/pressure/discomfort
  2. fatigue
  3. indigestion, early satiety, inability to eat normally, constipation
  4. urinary frequency/incotinence (recent)
  5. back pain/pressure/discomfort
  6. unexplained weight loss
49
Q

what is FIGO staging? (I-IV)

A

for primary ovarian and fallopian tube cancer

-international federation of gynocology and obstetrics

50
Q

risk factors for cervical intraepithelial neoplasm (CIN)

A
  1. > 1 sexual partner, or male partner with >1 sexual partner
  2. first intercourse at <18 years
  3. male partner with previous partner with cervical cancer
  4. smoking
  5. HIV infection, or previous STI
  6. solid organ transplant
  7. history of cervical cancer or HGSIL (high grade squamous intraepithelial lesion)
  8. infrequent or absent Pap screens
51
Q

what is the 2001 Bethesda system?

A

used to grade Pap smears for cervical cancers

MSII Pathology (11 decks)

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