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ENDO/REPRO > Concepts to Review > Flashcards

Concepts to Review Flashcards

1
Q

How can Primary polydipsia present ?

A

-Serum osmolarity: LOW
Urine osmolality : LOW
Na+ conc. :N/Low

-Water restriction >700mOs/L (urine)

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2
Q

First treatment SIADH?

A

-**Fluid Restriction. **

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3
Q

-A mass in sella turcica (pituitary adenoma) indicates what?

A

-Either Hypo/Hyper-pituitarism.
or compression mass

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4
Q

Why Hypothyroidism predisposed to prolactenemia?

A

-It will incr TRH–>incr Prolactine

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5
Q

Pre-couscious puberty?

A
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6
Q

Laron Dwarfisim?
Treat?

A

-GH recep mutation–>LOW IGF-1 –>HIGH GH levels
-Child is not growing for age–>give mescarmine (IGF-1 analog)
NOT A TUMOR..Neg feedback*

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7
Q

Diffrent prognosis:

Polydypsia,Polyruia (4)

A

-Nephrocalcinosis,Diabetus,DI,UTI’s

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8
Q

In Pituitary tumor, which will be most likly elevated?

A

-Prolactin

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9
Q

Thyroid development of cells?
Parafollicular
Follicular

A

-4th Pharyngeal pouch
-Endoderm

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10
Q

Cancers that spread hematogenously?

A

-Hepatocellular,Follicular Thyroid, RCC

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11
Q

Why amiodorone causes Hypothyroidism?

A

-Structure similarity of Thyroid H.

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12
Q

Tender thyroid?

A

Sub acute Granulomatosis Thyroditis.

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13
Q

Cretisisim ass(2)?

A

-Abnormal development (Agenesis, dysgenesis) or Abnormal thyroid H synthesis (due to thyroid peroxidase mutation)–>Dyshormonogenesis

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14
Q

What a.a is the precourser for Thyroid H?

A

Tyrosine is made from (phenylalanine).

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15
Q

Hyperthyroidism can cause what special ryttm?

A

-A.Fib (irregular-irregular Normal QRS )

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16
Q
A

OCP use:Total T4 increases–>you have incr TBG (bounded to T4)

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17
Q

Cold nodules
Hot nodules

In Iodine uptake test

A

-Adenoma/Carcinoma
-Graves/Toxic multinodular ..

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18
Q

Thyroid Carcinoma mut ass
Follicular
Papillary
Medullary
Anaplastic

A

-RAS (bone lesions–>fractures)

-RET, RET/PTC translocation,BRAF.Most important risk factor is past radiation exposure to neck.

-MEN2A ans 2B

-Tp53

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19
Q

CK increase in what thyroid disorder

A

-Hypothyroidism
Na/k+ inactivity

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20
Q

Why T4 is preferred over T3?
What situation is T3 prefferd over T4?

A

-Better binding to plasma globulins
-T3 is acute situations.

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21
Q

Cytokeratin-

Von Kossa-

C. Vimentin-

D. Congo red-

E. Desmin-

A

Cytokeratin-Epi tumor (squamous carcinomas)

Von Kossa- abnormal calcium deposits in the body. Papillary thyroid canrcinoma.

** Vimentin**-mesenchymal tissues (endometrial carcinoma,sarcomas,RCC,Meningioma)

Congo red-Amyloidosis

Desmin-Intermeadiate filaments (Sarcoma boitroides)–>Vaginal tumor//Muscle tumors (rhabdomyosarcoma)

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22
Q

Patient with Hashimotos develops a rapid growing mass, what most likly diagnosis?

A

-B cell Lymphoma.
-Dont confuse with anaplastic carcinoma–>compression sympt.

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23
Q

2 important microscopic presentations of Papillary carcinoma

A

-Psommoa bodies and orphan annie cells.

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24
Q

Location od thyroglssal cyst ?

A

Anterior neck mass,NOT in unilateral lobe.

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25
Q

Mass in neck.
Pleomorphic spindle shape cell?

A

-Anaplastic carcinoma thyroid–>20% ass pre-excisting Follicular carcinoma.

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26
Q

Meaning of exopthalmus and lid retraction?

A

Exophtalmus is sclera visible BELOW eye lids
Lid retraction is sclera visible ABOVE eye lids.

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27
Q

What stimulates Insulin release indirectly(2)?
and inhibit?

A

- Cortisol and Glucagon
-NE and Somatostatin

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28
Q

What 4 H. increase in Hyperglycemia?

A

-Epi., GH, Glucagon, Cortisol

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29
Q

Most common cause of death in patients with diabetus?

A

-MI due to Large vessel Non-enzymatic Glycation.

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30
Q

When you have insulin resistance–>what does your body do (3)?

A

-Promotes a Incr in glucose (all H come in)
1.Gluconeogenesis 2.Protein Lysis (weight loss),3. Lipolysis 4.Glycogenolysis–> polydysia,polyuria,polyphagia,weight loss

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31
Q

Patient that has Random glucose of >250 presents to clinic with normal apperance. Will you diagnose him as beaing Hyperglycemic?

A

-NO, you need hyperglycemic symptoms.

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32
Q

What does somatostatin control in pancreas?

A

-Alpha and Beta cells secretions.
-Inhibits cholecystokynin–>steatorrhea
Gastrin–>achlorydia (abd discomfort)..

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33
Q

In DKA what happens to K+ and Na+?

A

K+ moves to extracellular space, so you may find ir elevated in serum but reality is LOW –>being excrted.Thats why we say Reduced TOTAL K+ levels.
-Hypernatremia (volume depletion).

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34
Q

How do you describe Gross apperance of kidney in diabetus?

A

-Granular pattern with cortical atrophy

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35
Q

What is Insulin and C-Peptide level in Type 2 DM?

A

-Depends.They can be both increase or both decreased.

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36
Q
A
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37
Q

How to differentiate

17 alpha Hydroxylase
11 alpha Hydroxylasse
21 alpha Hydroxylase
Aromatase
Desmolase

A

-Only one with decr Sex H. (Female assymptomatic until puberty–>Amenorrhea)
-Incr BP and Decr K+ serum (11Deoxycorticosterone)
-Low BP and High K+ serum
-No electrolyte abn (K+ normal),Norml BP.
-Fatal

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38
Q

What does Cortisol do to FSH and LH?
-Where is it seen?

A

-Cortisol messes with GnRH secretions--> leads to *mesntrual irregularity (80%) *,amanorrhea,oligo.
Hirsutism, erectile dysfunction.
-Seen in Cushion syndrome.

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39
Q

Diagnosis

Patient untreated and has Graves and presents with infection–>develops Agitation,Confusion and Tachyarrythmias?

A

-Thyroid storm.
-4P’s

40
Q

Are hot nodules malignant?

A

-Rarley

41
Q

Patient with thyroid cancer opts for a total thyroidectomy. Weeks later, paresthesias and hyper-reflexia develop. What happened?

A

Removal of parathyroid glands–>HYPOCALCEMIA

42
Q

Most comm cause of HypoPTH is (3)

A

-Thyrodectomy. AIRE mut (autoimmune), Di-George syndrome.
-Spasm,parasthesia,Tetany

43
Q

Diagnosis

Low Ca++ levels,Short 3 and 4 digits,Dvelop delay and short stature??

A

-PseudoHypoPTH

44
Q

Where does PTH act?(3)

A

1.PCT (Na/Phosphate transporter)
2.DCT (Na/Ca++ Co-Transporter)
3.Osteoblast–>incr RANKL rel–>stimulates osteoclast.

45
Q

Diagnosis

Hypercalcemia
Hypophosphayemia
Hypercalciuria
-Excessive urination ,constipatin, flank pain , pain in bones ,and feeling depressed.

Complication??

A

-Excessive urination (Polydypsia)(Thrones),constipatin (Grones), flank pain (Stones), pain bones (Bones), and feeling depressed (psychyatric overtones)
-HyperPTH

-Osteitis Fibroda Cystica( made up of Hemossiderrin + Fibrous tissues) “Brown Tumor”

46
Q

-Most commm cause of Primary PTH,Secondary PTH??

-How to differentiate between Secondary HyperPTH between CKD and other and what complication may arise??

A

1= PTgland adenomas and SCC,RCC
2=CKD

-CKD–>HyperPHOSPHATEMIA (NO kidney function) +Hypocalcemia
Others: Hypophosphatemia
-Complication: renal osteodystrophy–>BONE LESION.

47
Q
A
48
Q

Diagnosis

pins-and-needles,” burning, tingling, and numbness in the distal extremities,temperature sensation, decreased vibratory sensation, and proprioception. Deep tendon reflexes are also diminished

A

-DM

49
Q

What is ass with Diabetic neuroptahy.

A

**Autonomic neuropathy **associated with diabetic neuropathy may result in *postural hypotension, arrhythmias, abnormalities of sweating, nocturnal diarrhea, gastroparesis, impotence, and bladder dysfunction. *

50
Q

What values constitutes microalbuminemia in urine in Diabetus mellitus??

A

-30-300mg/dL

51
Q

Mechanism on INSULIN

GH/IGF-1
Epi/NE

A

-Promote Insulin resistance,by decr glucose uptake
-In Glucagon

52
Q

Most used values for kidney Diabetus damage??

A

-Albumin:creatine ratio.

53
Q

What happens to K+levels in both DKA and HHS?

A

-DKA: Incr Extracellular K+ –>Total K+ loss(Ketones presents)
-HHS:Incr Intracellular K+ (NO Ketones)

54
Q

What is it?

Basement membrane thickening and protein leakage lead to nodular glomerulosclerosis and progressive proteinuria

A

Diabetus progression to Chronic Renal disease.

55
Q

hat is the consequence of small vessel disease in individuals with chronic diabetes mellitus in the retina?

A

Diffuse basement membrane thickening causes retinal hemorrhages, vessel proliferation, microaneurysms, and exudates

56
Q

3 common causes of Hypoglycemia in DM

A

1.Toxicity of Insulin secretants
2.Excessive exercise
3.No food intake while taking medications.

57
Q

Cortisol functiona?

A

-Maintains BP
-Stops division of Immune cells(Immuno supressors)
-Blocks neutrophils migrationn–>Neutrophilia
-Decr NFKB–>reduces TNF alpha,Lipoooxygenase, COX2.
-Incr glucose production in liver + reduces uptake in peripheral tissues.–>Diabetogenic effects.
-Incr lipolysis–>High cholesterol levels
-Decr bone formation (incr risk of fractures–>osteopenia/osteoporosis).
-Decr fibroblast–>poor wound healing–>thin skin (striea)
-Promotes adipocyte growth in central part of body.

58
Q

What 2 serum vamues are associated with Cushion syndrome beside cortiso and ACTH??

A

Hyperglycemia and Hyperchlomeria

59
Q

Diffrence treat of 1* and 2/3 adrenal insufficency??
-What do you see that RX dosent tell you?

A

-1–>need minerolocorticoid
2–>dont needed
3*–>glucoccorticoid abrupt stop

Hypoglycemia**

60
Q

Patient with low cortisol develops sepsis??

A

Addison crisis.Ass with meningiococcemia and bilateral adrenal hemorrage.

61
Q

Causes of 2* Hyperaldosteronism??

A

-Juxtaglomerular tumor (secrete renin), renovascular disease, CHF,Cirrosis,Nephrotic syndrome.

62
Q

Conn syndrome?

A

Primary Hyperaldosteronism (adrenal tumor)

63
Q

How do differentiate between 1 and 2 Hyperaldosteronsim?

A

-Differentiate due to Renin levels. amd given ACHE Inhibitor.

-Primary you do not have edema (Persistant Aldosterone escaoe mechanism)

64
Q

What are 4 hormones in Pheochromocytoma?
-Ass mutations?

A

-Epi,NE,Dopamine,EPO.
-VHL and MEN2A and 2B

65
Q

Vasoactive Intestinal Peptide Function??

A

Normal functions of VIP include increased secretion of water and electrolytes into the intestinal lumen and relaxation of intestinal smooth muscle and sphincters.

66
Q

What hormone out of 4 stress H (Glucagon,Epi.,GH, and Cortisol) does proteolysis?

A

Cortisol (loose weight).

67
Q

Why in Congenital Bilateral Hyperplasia codnitions all have bi lateral hyperplasia?

A

-Cortisol defc.–> ACTH incr–>Hyperplasia.

68
Q

Sympt. of Pheochromocytoma but empty medulla.Explanation

A

-Extra-adrenal (bladder,mediastainum).Do test to detect.
-Panic attacks is differential.

69
Q

organ of Zunckerkandl??

A

-Pheocrhromocytoma extra-adrenal in bifurcation of aorta.

70
Q

Diffrence between Pheochromocytoma and Neuroblastoma in amount of H produced?

A

-Pheochromocytoma= lots of cathelcolamine–>see them in urine.
-Neuroblastoma= inmature cells,dont see them in urine that much.

71
Q

What is Gestational diabetus??

A

-Mother has Diabetus Type 2–>Hyperglycemia–>passes it to fetus and fetus responds by HYPERPLASIA of Beta cells–>Hypoglycemia

72
Q

When symptoms of Type 1 DM start to appear and what do you see before sympt appear in microscipic image of pancreas?

A

-Start appearing after Beta cells are completly destroyed–>Insulin is normal.
-Before they are destroyed you see INSULINITIS

73
Q

What do you see in PTHgland-carcinoma?

A

-Ca++ levels are so high you definitly see Arrythmias.

74
Q

What mutations id Toxic mediated nodular Goiter ass??

A

TSH recep mutations. (60% cases).

75
Q

Why do patients with follicular carcinoma thyroid may have incr Iodine uptaje in other parts of body??

A

-This tumor metastasisez to bones and lungs–>expect Incr Iodine uptake in this regions.

76
Q
A
77
Q

Diffrence of 1* and 2* adrenal insufficency?

A

1*–> Adrenal inflamation (AIRE) and TB (resource pour countries)
metabolic acidosis, Hyperkalemia, LOW BP, Hypoglycemia, Hyperpigmentation

2/3–> Low ACTH secretion (compression adenoma or hypopituitarism)
Aldosterone is spared–> Hypokalemia,NO hyperpigmentation
Why you don’t need aldosterone treat.

78
Q

Why dysgenesis of thyroid in neonte dosen’t present with sympt?

A

-Mother has “passive immunity” towards child.

79
Q

What happens to TSH and T3 when giving amiadorone?

A

-Amiodorone mimmics T4 and inhibits 5’diodinase–>DECR T3 and INCR TSH

80
Q

What test do you do to diagnose Acromegaly?

A

-Oral glucose tolerance (72g within 2hr. it should supress it)

81
Q

Whats the classic triad of pheochromocytoma?

A

-Sweating,Tachycardia and headaches episodic.
**Hypertension <20yrs–>think Pheochromocytoma*

82
Q

Steps on diagnosing Cushions syndrome?
How to differentiate between Ectopic and Pituitary ACTH tumors physically?

A
  1. Do 24hr. urine cortisol, salivary night test, or LOW dose dexamethasone overnight.Just need 1 to determine Cushion (high cortisol).
  2. ACTH levels
  3. If ACTH is high–>HIGH dose Dexamethasone test.

-Ectopic has NO ACTH secretion.–>related peptide is decr (MSH).
**-Adrenal Cushion low ACT **

83
Q

What happens in preganacy to TSH, T4 and TBG?

A

TBG Incr
T4–>Incr
TSH–>decr.

hCH has similar alpha subunit–>esxplains
-Estrogen incr TBG

84
Q

Why do you see Hyponatremia in Hypothyroidism??

A

-Decr CO–> leads to ADH secretion–>fluid retention which may lead to hyponatremia

85
Q

From where does rT3 derive?

A

-From T4
-Both rT3 and T3 derive from T4.
-In hypothyroidism rT3 and T4 and T3 wiil be decr.

86
Q

What does excessive cortisol cause?

A

HyperTG, Hypercholesterol, Hyperglycemia, HyperBP,Immunosupression,Osteoporosis,Amonorrhea.

87
Q

What Thyroid Cancers are most likely to have hot nodules?

A

-The ADENOMAS
-Carcinomas are always cold nodules.

88
Q

Common presentation in patient with AIRE mut affecting parathyroid glands? What other endocrine abn may be present along side?

A

-Recurrent mucous-cutaneous candidiasis

May be ass with Addison disease.
Minerocorticoids defc-->hypotension,salt graving,hyponatremia
Glucocorticoid defc–>lowBP,fatigue,hypoglycemia,
Androgen defc.-->delayed pubic and axillary hair growth

89
Q

Loose Total Body K+ in what Diabetic emergency?

A

-BOTH

90
Q

VIPOMA explanation

A

-Promotes secretion into intestinal lumen–>excessive watery diarrhea every** even when fasting—>LOW BP**
-Also causes excessive K+ and Cl- secretion–>**Hypokalemia **and Hopychloremia.
-Incr bone resorption–>Hypercalcemia and Hyperglycemia.

91
Q

What does CK enzyme do?

A

**-Phosphorylates creatinine via taking Phosphate form ATP–>forms creatine-Phosphate—>stored for energy. **

92
Q

Granulomatous inflamation with multinucleated giant cells engulfing colloid

A

subcutaneous Granulomatous (Tender)

93
Q

What is Euthyroid sick syndrome?
How to diff with central hypothyroidism??
Do you treat??

A

-When a patient has a infection (non-thyroid related condition) and presents to hospital and when mesuring thyroid levels you see:LOW TSH, low T3, HIGH rT3.
**-Don’t treat it. Patient has **–>completly normal.
Central hypothyroidism and euthyroid is differentiated by rT3 levels, where normally rT3 will follow T4 levels.But in euthyroid it won’t.
-Very common to see it in hospitals.

94
Q

What other conditions is ass with MEN2B aside form medullary and mucosal neuromas?

A

-Marfan Habitus–>NO risk factor for aortic root dilation or ant **lens dislocation. **

95
Q

Usual presentation of Conn syndrome?

A

-Hypertension, Low renin, High aldosterone
Weakness (low K+), NO edema (Na++ inside BV dosent let H2O move outside), metabolic alkalosis

96
Q

Whats the mechanism of Aldosterone escape?

A

-As atrium fills and BP rises due to excess Aldosterone–>ANP is rel to eliminate excess water–>NO edema

ENDO/REPRO (10 decks)

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