UW 5 Flashcards

1
Q

What are PCOS women deficient in

A

Progesterone

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2
Q

What is happening with estrogen in PCOS

A

Unopposed estrogen

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3
Q

Pt complains that straight lines appear wavy
Test?
Si/sx’s?

A

Macular Degeneration

  • Grid test
  • Driving and reading - activities affected
  • Centrally located macula does fine visual acuity
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4
Q

When is enlarged blind spot seen

A

Papilledema

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5
Q

Karyotype and Presentation of Kallmann syndrome

A

Normal Karyotype: Female 46 XX, Male 46 XY
Normal genotype and internal productive organs
Absence of GnRH
- Females = Primary Amenorrhea, absent breasts
- Males = Eunuchoid, small external genitalia, absent secondary sexual traits - pubic hair, libido, deep voice
- Anosmia

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6
Q

Labs in Kallmann

A

Low FSH

Low LH

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7
Q

What is the cause of Secondary HTN in hyperthyroidism

A

Hyperdynamic state

  • increased expression of myocardial sarcoplasmic reticulum Calcium dependent ATP
  • Increased target organ sensitivity to endogenous catecholamines
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8
Q

Which kind of HTN in thyrotoxicosis

A

Predominantly Systolic

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9
Q

Hypothyroidism induced HTN

What kind and MOA

A

Diastolic

Increased SVR

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10
Q

Pathophys of thyroid level changes in pregnancy

A
  • hCG stimulates TSH receptor
  • Increased estrogen causes increase in production of TBG = increased TBG-bound T3 and T4, so total T3 and T4 are high
  • SO increase in TBG, total T3, T4
    Normal TSH, free T4, T3
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11
Q

Free air under diaphragm

A

Perforation

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12
Q

Porcelain Gallbladder
Presentation
TX

A
Calcium-laden GB
Bluish/brittle
Chronic Cholecystitis 
RUQ pain, mass
TX: Cholecystecomy to prevent GB Cancer = Adeno
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13
Q

Gallstone ileus
pathophys
DX
TX

A

Large gallstones cause fistula formation bt GB and small intestine. Gallstone enters and obstructs intestine
DX: Presence of air in biliary tract
TX: Surgery

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14
Q

TX for TTP

A

Emergent Plasmapheresis to remove autoabs and replace deficient enzymes

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15
Q

TX for hypercalcemia

A

Symptomatic moderate and severe > 12

  • IV Saline Hydration
  • Calcitonin
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16
Q

During fasting, what happens to glycogen levels

A

Drop in first 12 hours

GN kicks in, and after 24 hrs - main source of glucose

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17
Q

Main substrates for GN

A
  1. Gluconeogenic amino acids - Alanine is main one
  2. Lactate
  3. Glycerol-3-Phosphate - intermediate break down of adipose
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18
Q

Alanine is converted to?

A

Pyruvate in GN

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19
Q

Lactate is converted to?

A

Pyruvate in GN

From anaerobic glycolysis

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20
Q

Older children w intussusception
Etiology
TX

A

Pathological lead point
Meckel’s diverticulum MCC in GIT
TX: Surgical resection

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21
Q

MC malignancy of thyroid gland

A

Papillary thyroid cancer

- Best prognosis

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22
Q

Thyroid cancer w worst prognosis

A

Anaplastic

23
Q

Thyroid cancer from parafollicular C cells

Assn’s?

A

Medullary

- MEN 2a and 2b

24
Q

Central scotoma + afferent pupillary defect + changes in color perception + decreased visual acuity

A

Optic Neuritis

25
Q

Optic Neuritis Presentation

A
Ages 20-45
Females > 
Color perception changes
Rapid impairment of vision
MS
26
Q

Presentation of Anterior Uveitis

A

Eye - painful and red
Blurring of vision
Keratic precipitates

27
Q

Open angle Glaucoma Presentation

A

Gradual loss of peripheral vision
Tunnel vision
Cupping of optic disc

28
Q

Osteomalacia

Etiology

A

Defective bone mineralization of organic bone matrix
MCC Vit D deficiency
causes decreased intestinal calcium and phosphorus absorption w secondary hyperparathyroidism
Others: Malabsorption, Celiac sprue

29
Q

Labs of Osteomalacia

A

Hypophosphatemia
Hypocalcemia/Normal Ca
High Alk Phosp

30
Q

Etiology of GVHD

A

Host major and minor HLA Ag recognition by DONOR T cells and CMI

31
Q

Graft rejection

A

Mediated by HOST T cells

32
Q

Labs in premature ovarian failure

A

Low estrogen
High FSH, LH
FSH > LH

33
Q

Rubella Triad

A

Leukocoria
PDA
Hearing Loss

34
Q

Congenital Toxoplasma Triad

A

Chorioretinitis
Intracranial calcifications
Hydrocephalus

35
Q

Congenital Syphilis Presentation

A

Cataracts

Senso Hearing loss

36
Q

Risk factors for polyp progressing to malignancy (colon)

A

Villous adenoma
Sessile adenoma
> 2.5 cm

37
Q

Which type of polyp is non neoplastic and what is management

A

Hyperplastic

No further workup

38
Q

Test of choice for esophageal perforation

A

Water-soluble contrast esophagram

39
Q

Esophageal Perforation/Rupture Presentation

A

Worsening of condition after endoscopy

Radiographic findings - pleural effusion (L), pneumomediastinum, Pneumothorax

40
Q

Beck’s Triad

Infants?

A

Distant Heart sounds
Distended jugular veins
(Scalp veins in infants)
HypoTN

41
Q

Immediate postpartum, normal findings

A

Low grade fever
Leukocytosis
Lochia rubra, serossa, alba
Not foul smelling

42
Q

MC adverse rxn of blood trasfusion 1-6 hours

A

Febrile nonhemolytic transfusion

  • Fever
  • Chills
  • Malaise
43
Q

Prevention of febrile nonhemolytic rxn

A

Leukoreduction of donor blood - residual plasma and/or leukocyte debris remains in red cell concentrate which release cytokines during storage

44
Q

Urinary Cyanide test

A

Presence of cysteine

Think cystinuria

45
Q

Hep C patients being considered for TX - management

A

LIver BX - best clinical predictor of disease progression

Assesses response to TX

46
Q

Newly diagnosed Hep C patients

A

Assess for antiviral tx to delay progression w Liver BX

47
Q

TX for hep C

A

Peg-IFN

Ribavarin

48
Q

Electrolyte change with SAH

A

Hyponatremia

Cerebral Salt wasting syndrome

49
Q

Neuroimaging finding in Autism

A

Increased total brain volume

50
Q

Neuroimaging in OCD

A

Abnormalities in orbitofrontal cortex and striatum

51
Q

Neuroimaging in Panic disorder

A

Decreased volume of amygdala

52
Q

Neuroimaging of PTSD

A

Decreased hippocampal volume

53
Q

Neuroimaging in Schizophrenia

A

Enlargement of cerebral ventricles