Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ENRP > Week 4 (Exam 2) > Flashcards

Week 4 (Exam 2) Flashcards

1
Q

Cardiac support for patients unresponsive to conventional therapy until thyroid hormone normalization can be achieved

A

ECMO (extracorporeal membrane oxygenation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Autoimmune polyendocrine syndrome 2

A

Adrenalitis, thyroiditis, DMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Biggest causes of primary hyperparathyroidism

A

Adenoma is almost all of them

primary hyperplasia, 5-10%, parathyroid CA 1%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

MEN1

A 
Primary hyperparathyroidism
Pancreatic endocrine tumors
Pituitary adenomas (lacto- or somatotrophin)
Menin (MEN1) ts gene mutation
Can also have duodenal gastrinomas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Watch out for what in girls with delayed puberty or shortness

A

Karyotype (looking for 45 XO)

Turner’s comes with horseshoe kidney, CV defects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Burch Wartofsky Score

A

Thyroid storm: Fever, Cardiac (tach, CHF), GI (diarrhea, jaundice), Precipitating Hx (pregnancy, hemithyroidectomy, amiodarone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Signs and sx of Hyperglycemic hyper osmotic syndrome

A 
Glucose over 600
Severe dehydration
Hyperosmolality (over 350) - obtundation, coma
Impaired renal function
NO KETONES
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Etiology of congenital adrenal hyperplasia

A

21-hydroxylase deficiency (steroidogenesis)

impaired feedback to hypothalamus/pituitary with resultant hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Amiodarone dosing

A

200mg tab with 74.4mg I with 7.4mg released qd as free
Daily recommended I is 0.15mg
You can see why this can be toxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pseudohypoparathyroidism

A

Hypocalcemia, hyperphosphatemia despite high PTH
Physiology acts like its not even there
Resistance to PTH! related to G-protein receptor pathways, can affect other hormone paths (TSH,LH/FSH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Three main sources of hypopituitarism

A

Tumors (craniopharyngioma, Rathke’s, glioma)
Empty Sella
Sheehan: post partum necrosis of Anterior Pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Symptomatic vs Asx hypercalcemia

A

ASx means primary hyperparathyroidism

Sx means malignancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Leading cause of end stage renal disease in the US

A

Diabetic nephropathy. Screen it out with albumin:creatinine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Radioactive I for thyroid cancer

A

Contraindicated in pregnant women, its meant to target and destroy the thyroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Sx of Non-ketotic hyperosmolar state

A

Polyuria, thirst, altered mental state

ABSENT n/v, abdominal pain, kussmaul respirations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Hyperglycemic hyper osmotic syndrome

A

Acute hyperglycemic crisis in DMII

Culmination of prolonged insulin deficiency: Increased gluconeogenesis, decreased glucose uptake in peripheral tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Parathyroid adenoma

A

Benign neoplasm of parathyroid chief or oxyphil cells
Typically solitary, maybe surrounded by rim of normal parathyroid tissue
Come from MEN mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Pro-thyroid agents (4)

A

T4: Levothyroxine
T3: Liothyronine
Liotrix (4:1 mix of T4:T3)
Thyroid desiccated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Insulin indicated for post-prandial hyperglycemia

A

Glulisine
Taken before meal as SQ injection
Onset 5-10 min, lasts 1-3 hr, peaks 0.5-1 hour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Cells of the parathyroid

A

Chief Cells
Oxyphil Cells
Adipocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Best practices for evaluating pediatric growth

A

<36 mo w/ 0-36mo curve: measure while supine (length)

>36 mo w/ 2-20y.o. curve: measure standing up (stature)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

K replacement in DKA

A

When serum K is below 5.5

Monitor for cardiac changes and verify urine output (probs need indwelling foley)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

DiGeorge Syndrome

A

22q11.2 deletion
possibly parathyroid under- or non-development
Causes hypocalcemia
Facial anomalies, “tet spell” cyanosis, tetany, infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Tertiary hyperparathyroidism

A

Prolonged hypocalcemia causing autonomous function of parathyroid glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Fluid replacement protocol for DKA

A

2-3 liters normal saline (first 1-3 hrs)
then half-strength saline at 150ml/hr
Once glucose hits 250, switch to 5% dextrose 0.45% saline at 100-200ml/hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Papillary thyroid carcinoma

A

Majority of malignant thyroid tumors, 25-50 years old
Usually Asx, palpable nodule, seen on US
Psammoma bodies, “orphan Annie eye nucleus” is Dx
RET-PTC and BRAF mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Levothyroxine MOA

A

Manufactured form of T4, converted to T3
Can take up to 6 weeks for max effect
Dosing based on regular TSH and T4 measurements
Sides: weight loss, sweating, anxiety, etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Calciphylaxis

A

Secondary hyperparathyroidism causing calcification and occlusion of blood vessels with resultant ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Signs and Sx of DKA

A 
Abdominal pain, mental dysfunction, coma
Kussmaul (rapid/deep) Respirations
Fruity or nail-polish breath
Dry mucous membranes, poor skin turgor
Fluid deficit 3-5L (less than NKHS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Anti-thyroid agents (4)

A

Radioactive iodine (131I) sodium
Methimazole
K-Iodide
Propylthiouracil (PTU)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Treat thyrotoxicosis (thyroid storm, symptomatic hyperthyroidism)

A

Non selective b-blocker (1 and 2): inhibit conversion of T4 to T3 (more biologically active version in periphery)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Somatostatinoma

A

Diabetes, cholelithiasis, steatorrhea

Reduced insulin, reduced gallbladder motility, reduced exocrine pancreas secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What nerve transmits referred pain from the spleen to the shoulders?

A

Phrenic (Kehr’s sign)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Presentation of DKA

A

Triad of hyperglycemia, ketonemia, metabolic acidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

How does graves disease cause exophthalmos

A

lymphocytes invade preorbital space, fibroblasts there have TSH receptor. EOM swells, matrix accumulates, adipocytes expand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Metformin MOA

A

Activates AMP-activated protein kinase

biguanide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Gliflozin clinical uses

A

Adults with DMII, taken orally before first meal qd

Correct hypovolemia before starting this

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Empty Sella Syndrome

A

Primary: SCF leaks into it, compresses pituitary
Secondary: Pituitary expands and infarcts within sella

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Meglitinide clinical use

A

postprandial hyperglycemia, oral before meal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the purpose of radioisotope scanning goiters?

A

Determines if a nodule is responsible for hyperfunction
Cold nodules are more likely neoplastic (hot more likely to be benign), but US and fine needle aspiration are more useful

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

MEN2a

A

Pheochromocytoma
Medullary thyroid carcinoma
Parathyroid hyperplasia
Germline RET proto-oncogene GOF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Glulisine MOA

A

Mutations from human sequence block assembly of dimers and hexamers - allow for faster glucose absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

C Cells

A

In the thyroid, make calcitonin

NE carcinoma have amyloid, blue w/ chromatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Sx of primary hyper parathyroidism

A

Painful Bones (osteoporosis/osteitis fibrosis cystica)
Renal Stones
Abdominal groans (constipation, stones)
Psychic moans (depression, lethargy, seizures)
These are mostly from protracted Hypercalcemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Diagnostics of 21-hydroxylase deficiency

A

Heel stick the baby!
ACTH stimulation test
17-hydroxyprogesterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Somatotroph pituitary adenoma histology

A

Like all adenomas there’s diffuse growth. These can be mixed with PRL-secreting cells though

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Hormone levels found in primary hyperthyroidism

A

Decreased TSH, Increased FT4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Steps of insulin release

A

GLUT-2 takes it into b-cells, generates ATP, inhibits K channel, causes Ca influx, causes insulin release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Glargine MOA

A

aa substitutions in both a- and b-chains enhance crystal stability, changing the pKa of insulin
for basal maintenance, 1-2 SQ daily
Onset 3-4 hours, lasts 24 hours, peakless

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

K-I MOA

A

Stable form of iodine, blocks its uptake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Labs of Grave’s disease

A

T3/T4 high
TSH low
TSI (thyroid stimulating Ig) High

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Gliptins

A

Sitagliptin, Linagliptin, Saxagliptin, Alogliptin
Inhibit DPP-4, a serine protease that degrades GLP-1
Mono or combo with metformin/sulfonylureas/TZDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Adverse effects of metformin

A

GI complications: anorexia, N/V, etc
Lactic acidosis, esp w/ hypoxia, renal and hepatic insufficiency
Contraindicated in conditions predisposing to tissue hypoxia (HF, COPD, renal failure, alcoholism, etc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Indications for Propothiouracil (PTU)

A

Patients w/ Graves, toxic multi-nodular goiter, methimazole intolerance, surgery or rads not happening
Ameliorates hyperthyroidism sx
Preps for thyroidectomy
Used in rad I therapy w/ methimazole intolerance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Main function of the parathyroid

A 
Calcium homeostasis via PTH, affecting kidney: 
Ca resorption (blocks Phos resorption), activates vit D
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

DKA vs HHS

A

DKA pH is below 7.3, HHS is above
DKA HCO3- is below 18, HHS is above
DKA osmolality is below 320, HHS is above
HHS hyperglycemia is above 600, DKA is above 250

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What stimulates the release of endogenous incretins?

A

Oral glucose, activated by DPP-4

The two ones are GLP-1 and GIP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Thyroid acropachy

A

In severe cases of Thyroid dermopathy (pretibial myxedema, non-pitting edema or plaques)
Soft tissue swelling, clubbing of fingers and toes, periosteal reaction of bones of hands and feet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Partial deficiency of 21-hydroxylase

A 
Simple virilization (without salt wasting)
Nonclassic / late onset
Precocious puberty, acne, hirsutism at puberty
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

MODY

A

Looks like DMII but happens in youth
Increased blood insulin, no Abs, nonketotic
Usually from Glucokinase LOF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Clinical use for regular insulin

A

Basal maintenance
Overnight coverage
Post-prandial hyperglycemia (inject 45 min prior)
IV when urgent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Most common cause of death in diabetics

A

MI

also at increased risk of stroke, MI, leg gangrene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Tigger CaSR mutation

A

GOF, Thinks there’s plenty of Ca when there isn’t
Turns off PTH (hypocalcemia)
increases renal excretion (hypercalciuria)
AD HypoPTH (hypercalciruic hypocalcemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

HAGMA differential

A

Methanol, Uremia, DKA!, Paraldehyde, Isopropyl alcohol, Lactic acidosis, ethylene glycol, salicylates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Zollinger Ellison Syndrome

A

caused by G cell gastrinoma
Islet cell tumor + Gastric acid hyper secretion + Peptic ulceration
Do not respond to clinical diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Non-neoplastic causes of hyper-prolactinemia

A

Pregnancy, nipple stimulation, Renal Failure, Hypothyroid
Loss of DA: Lactotroph hyperplasia (neuron damage, drugs like Verapamil, Metoclopramide, antipsychotics or antidepressants with blockade of DA recs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Incretin MOA

A

GI hormones that decrease blood glucose
Activate GLP-1 receptor or boost it
Synthesized by L-cells
Promote b-cell proliferation, insulin gene expression, glucose-dependent insulin secretion
Inhibit Glucagon secretion
Inhibits gastric emptying (causing satiety)
Short half life, not an effective drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

How do thiazolidinediones cause osteoporosis

A

Uses PPARy to direct mesenchymal stem cells away from osteoblast/Runx2 path and toward C/EBPs/Marrow adipocyte pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Where are peptic ulcers most oftenly found?

A

Duodenum or stomach

Can perforate and cause free air in abdomen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Drugs that impair levothyroxine absorption

A

Antacids, Iron, Sucralfate (anti-ulcer), Cholestyramine!, orlistat, PPIs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Treatment of hyperthyroidism

A

Tx Sx w/ b-Blockers

Tx Dz w/ high dose iodide (Wolff-Chaikoff effect), thionamide, radio iodine ablation, surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Transcription factors associated with pituitary adenomas

A

Most functional are associated with PIT-1

Exception: corticotroph adenoma, TPIT associated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Retinal findings of diabetes

A

Cotton-Wool spots
VEGF-caused neovascularizations
Cataracts, glaucoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Rugger Jersey Sign

A

Lots of space between vertebral discs
Renal Osteodystrophy
Dissecting osteitis in hyperparathyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Follicular Adenoma of the thyroid

A

Discrete clonal population of follicular cells with “thyroid autonomy”
Benign, but make sure the capsule is intact (not invaded) and there’s no nuclear features of papillary CA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Conn’s Syndrome

A

Primary hyperaldosteronism
HTN (refractory/adrenal mass/young/severe)
Hypokalemia
Hypomagnesemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Pramlintide

A

Amylin analog, likely at CNS receptors
Rapid onset, 3 hours duration, 20 min peak
DMI, DMII pts who take mealtime insulin
Injected SQ before meals as insulin adjunct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

NPH MOA

A 
Complex of protamine with zinc insulin
Basal maintenance / overnight. Not used much.
Onset 1-2 hours
Duration 10-12 hours
Peaks in 4-12 hours
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Insulin requirements in nephropathy has gastropathy

A

Gastropathy: pacemaker dysfunction makes absorption and insulin need variable
Nephropathy: if they’re dysfunctional, they don’t clear insulin, so the requirement goes down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

HLA typing of DMI

A

DR/DQ on Chr 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Clinical use of thiazolidinediones

A

DMII, delays its progression

No hypoglycemia when used alone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Craniopharyngeoma

A

Kids: adamantinomatous, growth retardation from hypopituitarism
Adults: papillary, increased intracranial P or hypopituitarism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

TRH function / cascade

A 
Thyrotropin releasing hormone
From hypothalamus when BMR falls
Triggers TSH release from hypophysis
Stimulates Thyroid to release TH (3 and 4)
MBP increases and suppresses further TRH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Regular insulin MOA

A

Unmodified zinc insulin crystals
Onset 0.5-1 hour
lasts 10 hours
Peaks in 3-5 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Growth velocities by age groups

A

below 4: at least 7cm/year
4-6: at least 6cm/year
6+: 5cm/year!! (2 inches)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Thyroid storm presentation

A

Extreme and abrupt episode of potentially life threatening thyrotoxicosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Identify an aldosterone secreting adenoma

A

Spironolactone bodies

Small, young pts, much ischemic heart dz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Nelson Syndrome

A

A Cushing’s patient gets their adrenals removed, so then they get an enlarged pituitary (trying to compensate) and adenomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Amylin analog MOA

A

OG is pancreatic and synth by b-cells

Enhances action of insulin via inhibiting glucagon synth, decreased gastric emptying, causing satiety

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Adverse effects of thiazolidinediones

A

Weight gain
Edema: increase vascular permeability, ENaC (increased Na and H2O reabsorption in collecting duct)
Worsens HF b/c water retention
Osteoporosis: Direct MSCs to adipocyte diff’n, suppress diff’n of MSCs into osteoblasts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Thiazolindinediones

A

Pioglitazone and rosiglitazone
PPARy ligands (nuclear receptor in fat, muscle liver, endothelium)
Increase GLUT4 in skeletal m. and fat, IRS1/2/PI3K
Decreased PEPCK, NF-kB, AP-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Thioamide medications (3)

A

Propylthiouracil (PTU)
Methimazole
Carbimazole (converted to methimazole, 10x more potent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Thioamide MOA

A

Blocks iodide organification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Eeyore CaSR mutations

A

LOF, thinks there isn’t enough Ca when there is
Turns on PTH (hypercalcemia)
Reduces renal excretion (hypocalciurea)
Familial Hypocalciuric Hypercalcemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Criteria for puberty being precocious

A

Full activation of HPG axis: girls at 8 years old, boys at 9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Adverse effects of supplemental insulin

A

Lipodystrophy (fat hypertrophy: switch up injection site)
Resistance (via IgG abs to insulin)
Allergic Rxn
Hypokalemia
Hypoglycemia (from missed meal, exercise, OD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Subacute lymphocytic thyroiditis

A

Transient period of thyroid hormone irregularities
Hypo- (sometimes hyper-)thyroidism
Goiter
Ex. Post-partum thyroiditis, can progress to permanent hypothyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Clinical uses of a-glycosidase inhibitors

A

DMII as mono therapy or combo
Oral at mealtime
Doesn’t cause hypoglycemia when used alone
Dont cause weight gain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Osteitis Fibrosis Cystica (von Recklinghausen’s dz)

A

Starts as Brown Tumor

Osteoclast-driven bone destruction, small fractures, hemorrhage and reactive tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Sx of diffuse, non-toxic Goiters

A

Often euthyroid, sx due to mass effect: dysphagia, hoarseness, stridor, SVC syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Sx of primary acute adrenocortical insufficiency

A

Adrenal crisis: rapid withdrawl of steroids
Massive adrenal hemorrhage (Waterhouse-Friderichsen)
Stress, infection, trauma, burns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Autoimmune polyendocrine syndrome 1

A

AIRE mutation
Adrenalitis, parathyroiditis, hypogonadism, pernicious anemia, mucocutaneous candidiasis (anti IL-17 and 22 Abs), Ectodermal dystrophy (fucked nails and teeth)
APECED

103
Q

familial mutations associated with pituitary adenomas

A

AIP (FIPA): Somatotrophic, PAP/pituitary adenoma predisposition

104
Q

Guidelines for DMII monitoring

A

Quartlerly A1c, Glucose monitoring review, foot check

Annual eye exam, micro albumen:creatinine, monofilament testing

105
Q

Anterior hypopituitarism

A

No Growth hormone, gonadotropins, TSH, Adrenocorticotrophic hormone, prolactin

106
Q

Albright’s hereditary osteodystrophy

A

Short stature, fingers, toes, obesity
Dental abnormalities, subQ ossification, cataracts
sometimes seizures and tetany

107
Q

Hormone levels found in primary hypothyroidism

A

Increased TSH, decreased FT4

108
Q

Most telling sign of parathyroid carcinoma

A

Elevated PTH that doesn’t go down after surgery (mets)

109
Q

General adrenal medulla physiology

A

Made of chromatin cells from NCC

Do epi and norepinephrine from sympathetic control

110
Q

Sulfonylurea MOA

A

K(atp) channel blocker
Bind to SUR1 sulfonylurea receptor
Blocking K+ current through Kir6.2 inwardly rectifying K channel

111
Q

Pramlintide Adverse effects

A

N/V, vomiting, diarrhea, anorexia
Severe hypoglycemia if used w/ insulin
Enlaces anticholinergics on GI (constipation)

112
Q

SIADH

A 
Mental status changes, weakness, seizures
From small cell lung CA, Brain injury, Drugs (SSRIs)
Inappropriate thirst (unlike DI where you actually need water)
113
Q

Therapeutic options for follicular carcinoma of the thyroid

A

Surgery, radioactive iodine

Refractory: Chemo, TK inhibitors

114
Q

Mechanisms of Hypercalcemia in malignancy

A

Humoral Hypercalcemia of Malignancy: PTHrP (PTH analog, squamous carcinomas), Vit D mediated (lymphomas)
Local Osteolytic Hypercalcemia: release of Ca (osteoclastic bone resorption, breast CA, myeloma)

115
Q

Treatment for Somatotroph pituitary adenoma

A

Somatostatin analogs or GH antagonists or surgery

116
Q

Hormone levels found in TSH producing tumor

A

Increased TSH, Increased FT4

117
Q

NKHS treatment

A

Regular insulin 5-10 units IV bolus
3-7 units continuous infusion (transition when eating)
Monitor and replace K just like in DKA

118
Q

General adrenal medulla physiology

A

Made of chromaffin cells from NCC

Do epi and norepinephrine from sympathetic control

119
Q

Types of Pituitary adenoma cells

A

Lactotroph (prolactin), Somatotroph (growth hormone), Corticotroph (ACTH), Thyrotroph (TSH), Gonadotroph (LH/FSH)

120
Q

MEN2b

A

Mucosal neuromas
Marfanoid body habitus
PHeochromocytoma
Medullary thyroid CA (RET oncogene)

121
Q

How are thyroid hormones made?

A

Tg (thyroglobulin) synthesized and stored in colloid
Iodide is transported into cell, incorporated into Tg
Tg endocytose and cleaved to released T3 and T4

122
Q

Pharmacokinetics of thiazolindinediones

A 
Delayed onset (1-3 months), persist weeks-months
Metabolized by the liver: half life reduced by CYP inducers (rifampin) and prolonged by CYP inhibitors (gemfibrosil)
123
Q

CaSR

A

Calcium sensing receptor of parathyroid gland that regulates PTH

124
Q

Sulfonylurea adverse effects

A

Hypoglycemia, weight gain, secondary failure (patients who respond initially later cease to respond to sulfonylureas and develop unacceptable hyperglycemia)

125
Q

How to diagnose pheochromoctoma

A

Urine and plasma metanephrines

126
Q

Dexamethasone Suppression test

A

Cortisol level suppressed after high dose = Cushing’s
Corticotropin suppressed = adrenal tumor/hyperplasia
No suppression at all = ectopic corticotropin source

127
Q

Best practices for evaluating premature baby growth

A

Adjust for height and weight for first 2 years

Plot gestational, not chronological age for first 2 years

128
Q

Use insulin to manage severe hyperkalemia

A

Insulin + glucose + Furosemide
Glucose prevents hypoglycemic shock
Insulin activates Na/K-ATPase shifting K+ into cells
Effect is transient, so eliminate the K w/ Loop diuretics

129
Q

Clinical findings of pituitary lesions stemming from mass effect

A

Papilledema, bilateral temporal hemiano ia
Pituitary Apoplexy (hemorrhage into adenoma)
Underproduction of hormones (except prolactin!!)
HA, N/V, HTN, bradycardia, shallow breathing

130
Q

Liraglutide

A

GLP-1 analog with 97% homology
Lipid modified: rapidly absorbed but binds to albumin
Half life is 11-15 hours

131
Q

Histology of craniopharyngiomas

A

From rathke’s pouch remnants
Squamous epithelium
“wet” keratin
Calcified cyst

132
Q

Initial monitoring of DKA

A

Blood glucose at least hourly
Electrolytes q2-4h
Clinical status at least hourly

133
Q

Insulin metabolic pathways

A

Activates MAP kinase (cell growth, etc)

Activates PI-3K (synthesis/survival and GLUT4)

134
Q

Estimate the height a child will reach

A

Height at age 2 x2
Mid-parental: Boys: [(dad + mom) +5] 2
girls: same but minus 5. This is all in inches, btw

135
Q

Etiology of DMI

A

Failure of T self-tolerance against b-cells

MHCII susceptibility on HLA DR/DQ Chr6p21

136
Q

Hyperthyroidisms

A

Primary (most common): graves, hyperfunctioning multi nodular goiter, hyperfunctioning thyroid adenoma
Secondary hyperthyroidism from pituitary adenoma
Distinguish: primary has Low TSH, secondary is High

137
Q

Secondary Hyperparathyroidism

A

Hypocalcemia from renal failure, gastric bypass, vit D def, pseudo-hypoPTH
Causes increased parathyroid volume adaptively

138
Q

Growth hormone deficiency findings in neonates

A

Midline defects, microcephalus, hypoglycemia

GH not relevant for growth during first year of life

139
Q

First and second gen sulfonylureas and non-sulfonylureas (meglitinides)

A

1: Chlorpropamide, Tolbutamide, Tolazamide
2: Glipizide, Glyburide, Glimepriide
Non: Nateglinde, Repaglinide

140
Q

Premature Thelarche

A

Palpable glandular tissue in girls below 2

Increased over 4-6 mo period

141
Q

Fluid replacement in NKHS

A

2-3 liters NS over first 1-3 hours
Fluid deficit 8-10L (reverses in 24-48 hours w/ 0.5 NS)
Glucose reaches 250 switch to d5halfNS 100-200qh

142
Q

Findings indicative of precocious puberty

A

Girls: progressive breast development,
Boys: testicular and penile enlargement
Both: crossing major percentile line upward on linear growth chart

143
Q

Primary vs secondary adrenocortical insufficiency

A

1: loss of cortical cells, hormonogenesis defect
2: HPA suppression by extra-adrenal steroid source

144
Q

Distinguish PTH vs VIt D issue

A

PTH: Ca and PO4 go in opposite directions

Vit D: they go in the same direction

145
Q

Genetics of Follicular carcinoma of the thyroid

A

PAX8-PPARG (less than 10% are positive)

146
Q

Adverse effects of a-glycosidase inhibitors

A

Malabsorption, flatulence, diarrhea, abdominal bloating

hypoglycemia when combo’d w insulin/secretagogues

147
Q

Goitrogens

A

Diffuse, non-toxic goiters
Cassava root (thiocyanate)
Brassicaceae (broccoli, cauliflower, cabbage, radish)

148
Q

Follicular variant of papillary thyroid carcinoma

A

Follicular architecture with nuclear features of papillary

More have RAS mutations (like follicular CA or Adenoma)

149
Q

Findings of complete 21-hydroxylase deficiency

A

Salt Wasting: no mineralocorticoids or cortisol
Hyponatremia, Hyperkalemia, HPTN
Female virilization (at birth)
Long term HPTN
Adrenogenital syndrome (cliteromegaly, fused labia)

150
Q

Why does chronic adrenal insufficiency cause skin hyperpigmentation?

A

Corticotropin releasing hormone tries to compensate by stimulating all this POMC to get it converted to ACTH but also MSH!! (melanocyte stimulating hormones)

151
Q

Findings indicative of premature adrenarche

A

Increased DHEA/-S
Appearance of pubic and axillary hair, odor, acne
Normal growth and genitalia

152
Q

Gliflozins

A

Inhibit SGLT2 glucose reabsorber in PCT
Canagliflozin, Dapagliflozin, Empagliflozin
Turns complete glucose reabsorption to just partial

153
Q

Genetics of follicular neoplasms of the thyroid

A

RAS and PTEN

154
Q

de Quervian’s thyroiditis

A

Granulomatous - painful, maybe viral
Sometimes lumped in with subacute thyroiditis
Hypo- or Hyperthyroiditis

155
Q

Hormone levels found in Central hypothyroidism

A

Decreased TSH, Decreased FT4

156
Q

Hypercalcemia on EKG

A

Shortened QT interval

157
Q

Genetics of anaplastic carcinoma

A

TP53

158
Q

24 hour urine collection in diabetic patients for protein and creatinine clearance

A

Need serum creatinine at the same time to determine clearance
Its difficult to save all urine

159
Q

Presentation of DMI in a baby

A

Polyuria, Polydipsia, lethagy, weight loss, extreme hunger

160
Q

Cells of the endocrine pancreas

A

D1: Secretes VIP (vasoactive intestinal polypeptide)
Delta: somatostatin
PP: pancreatic polypeptide

161
Q

DEXA scan scoring

A

Normal is -1 or higher
Osteopenia is -1 to -2.5
Osteoporosis is less than -2.5 (severe w/ fracture)

162
Q

Microalbumen:Creatine

A

Random urine sample
More accurate than micro albumin alone because it corrects for variations from [urine]
Microalbuminuria = 30-300mg

163
Q

Most additive risk for vascular disease

A

SMOKING

164
Q

Myxedema

A

Hypothyroidism in the adult/older child
Mental and physical sluggishness
Weight gain, cold intolerance, cardiac effect (lower output, hypercholesterolemia)

165
Q

Cushing’s syndrome vs disease

A

Disease is from a pituitary corticotroph adenoma
Syndrome can come from many other things
Both have abdominal striae, thin skin, hirsutism, etc

166
Q

Initial insulin administration for DKA

A

10-20 units IV, the 5-10 per hour continuous IV

Increase if no response in 1-2 hours

167
Q

Medullary thyroid carcinoma

A

Sporadic: Most common, univocal, aggressive, 50y.o.
Familial: 100% 15-year survival, multifocal, 43 y.o.
Ass’d w/ RET oncogene on chr 10
From C Cells (Calcitonin)
Polygonal-to-spindle shaped cells forming nests in trabeculae
Amyloid!

168
Q

Pharmacokinetics of metformin

A

Half life 1.5-3 hours

Not bound to plasma proteins, not metabolized, excreted unchanged by kidneys

169
Q

Graves disease

A

Hyperthyroidism with gland enlargement
Infiltrative opthalmopathy (can have lines on eyes)
Pretibial Myxedema

170
Q

Acute vs chronic adrenal insufficiency sx

A

Acute: HPTN, abdominal pain, N/V, Hypo-N/Glycemia
Chronic: malaise, joint pain, hyperpigmentation

171
Q

Riedel thyroiditis

A

Fibrosing, extends from thyroid to adjacent tissue
Feels like cement
Lots of lymphocytes and plasma cells
IgG4-related, EUTHYROID

172
Q

Why taper steroids tp treat adrenocortical insufficiency

A

Can cause adrenal atrophy

173
Q

Criteria for delayed bone age

A

Two SD below chronologic age, assessed by ossification of epiphyseal centers

174
Q

Propothiouracil MOA

A

Inhibits synthesis of thyroid hormones in hyper-
Inhibits thyroxine to triiodothyronine conversion peripherally
Does not inactivate pre-existing T3/4!
Does not interfere with given hormones!

175
Q

Histology of Hashimoto thyroiditis

A

Atrophic follicle cells with eosinophilic change (Hurthle cell metaplasia)

176
Q

Treatment for lactotroph adenoma

A

DA agonists (bromocriptine, Cabergoline), surgery

177
Q

What Abs would you expect to find in DMI?

A

Islet auto-abs: Anti-insulin, GAD, ICA512

178
Q

How to attenuate the glucose-lowering effects of sulfonylureas

A

Inhibit insulin secretion: b-blockers, CCBs

Induce hepatic CYPs: Phenytoin, griseofulvin, rifampin

179
Q

Gonadotrophic pituitary adenoma presentation

A

Minimal function, often silent maybe with only mass effect

180
Q

Advantages of metformin

A

really good, doesn’t cause hypoglycemia or weight gain, oral, alone or in combo, decreased risk of macro- and microvascular complications in diabetic pts

181
Q

DKA treatment goals

A

Increase rate of glucose utilization (150-250)
Reverse ketonemia and acidosis
correct depletion of water and electrolytes

182
Q

Diabetic Gastropathy

A

Autonomic neuropathy where gastric pacemaker becomes too variable. Nutrient and glucose requirements become extremely variable too

183
Q

Presentation of hyperthyroidism

A

Lid lag, exophthalmos
Bruits over thyroid
Goiter, nodules, Tremor, warm skin, Gyno, weakness

184
Q

MODY

A

Looks like DMII but happens in youth
Increased blood insulin, no Abs, nonketotic
Usually from Glucokinase LOF

185
Q

Side effects of gliflozins

A 
Osmotic diuresis
Weight loss
Reduced BP
Reduced plasma Uric acid
Dont cause hypoglycemia when used alone
186
Q

Bilateral cortical hyperplasia

A

Expected in ACTH dependent Cushing syndrome (secondary)

187
Q

Follicular Carcinoma of the thyroid

A

Less common unless there’s iodide deficiency
PAX8/PPARG mut are characteristic (RAS less so)
Invaded (mushroom) capsule
Angioinvasion
Still considered differentiated thyroid CA

188
Q

Clinical presentation of apathetic hyperthyroidism

A

older adults with masked sx
unexplained weight loss
Cardiovascular disease

189
Q

Types of Insulin by speed

A

Rapid: Aspart, Lispro, Glulisine
Short: Regular
Intermediate: NPH
Long: Detemir, Glargine

190
Q

Exenatide

A

Recombinant exendin-4 w/GLP-1 activity

Modified Gila monster saliva, less susceptible to hydrolysis by DPP-4

191
Q

VIPoma

A

D1 cells, intestinal fluid secretion
WDHA syndrome: watery diarrhea, hypokalemia, achlorhydria
20% have flushing as well

192
Q

Endogenous factors of insulin secretion regulation

A

Glucose and other energy substrates
GPCR-Gs ligands: b2-AR and GLP-1 agonists (incretins)
GPCR-Gi ligands: somatostatin, a2-AR agonists

193
Q

Etiology of secondary hyperaldosteronism

A

RAAS: diuretics, bad renal perfusion, arterial hypovolemia, pregnancy, renin-tumors

194
Q

What pediatric patients do you send for referral?

A

Hight below 3rd or above 95%
Above 5cm/2in variance from mid-parental height
Bone age fast or slowed by above 2 SD
Abnormal growth velocity, dysmorphic features

195
Q

Somatic mutations associated with pituitary adenomas

A

USP8: corticotrophic, up regulates EGFR
GNAS: somatotroph. Makes a-subunit of Gs lose GTPase activity, proliferation cascade is constantly active

196
Q

Adverse effects of Gliflozins

A

HPTN, hypovolemia
Hypovolemic pts: ortho HPTN, dizziness, syncope
Genital and UTI
Hypoglycemia if combo’d w/ insulin or secretagogues

197
Q

Detemir MOA

A

Lys29 in b-chain is myristoylated (lipid: rapidly absorbed into blood but binds strongly to albumin)
Peaks in 3-9 hours

198
Q

Pheochromocytoma presentation and distribution

A

Profound HTN from adrenal tumor
Triad of HA, palpitations, Diaphoresis
10% are extra-adrenal, bilateral, pediatric, malignant, non-HTN associated
25% are familial

199
Q

C-peptide

A

Co-product of insulin creation

Marks endogenous insulin (can differentiate from pharmaceutical)

200
Q

Histologic difference between parathyroid hyperplasia and parathyroid adenoma

A

Hyperplasia does not have that normal rim of parathyroid tissue
One gland affected is adenoma, all means hyperplasia

201
Q

Rathke’s cleft cyst

A

During development, neck pf pouch constricted by mesoderm and pinches it off.
Can expand and compress normal pituitary
Can rupture and cause inflammation of pituitary, meningitis

202
Q

What do incretin mimetic do in addition to long-acting GLP-1 receptor activation?

A

DPP-4 inhibition (usually inactivates GLP-1)

203
Q

What are the two long-acting GLP-1 receptor agonists?

A

Exenatide and Liraglutide

204
Q

Etiologies of non-ketotic hyperosmolar state

A

Insulin deficiency, inadequate fluid intake, osmotic diuresis from hyperglycemia

205
Q

Pineal gland function

A

Produces melatonin, made from photoreceptor containing neural tissue

206
Q

Insulinoma

A

Small tumors causing hypoglycemia, often have amyloid. Dx via C peptide

207
Q

Possible damage done during thyroid surgery

A

Recurrent laryngeal nerve

Damage to parathyroid glands

208
Q

K-I indications

A

Treats hyperthyroidism, I deficiency, combo’d w/ other anti-thyroids to prep for surgical removal
Protects thyroid from radiation, shrinks it to reduce hormones (spares Cardio stuff)

209
Q

Methimazole MOA

A

Inhibits thyroperoxidase (normally catalyzes T3/4 synth)
Taken before thyroid surgery to lower hormone levels
Minimizes effects of thyroid manipulation

210
Q

Hashimoto Thyroiditis

A

Abs against thyroglobulin and thyroid peroxidase (TPO)
Diffuse, painless enlargement
Hypothyroid (except in hashitoxicosis)

211
Q

Growth hormone deficiency in children

A

Decreasing growth velocity
Low IGF-1 and IGFBP-3
Low GH levels during stimulation test (Insulin, Argenine, Clonidine)

212
Q

a-Glycosidase inhibitors

A

Acarbose and Miglitol
Competitive inhibitors of GI epithelium enzymes
Lower postprandial hyperglycemia for insulin-sparing

213
Q

Diffuse sclerosino variant of papillary thyroid carcinoma

A

Younger patients, more mets to lung, brain, bone, liver
Shorter periods of disease-free survival
Mortality comparable to those of conventional PTCs (93% survival at 10 years)

214
Q

Manage 21-hydroxylase deficiency

A

Glucocorticoids (does negative feedback for ACTH suppression, no more androgen over-stim)

215
Q

PTH is high but Ca is low

A

Secondary Parathyroid hyperplasia, typically 4-gland hyperplasia

216
Q

Fasting plasma glucose, two-hour glucose, and A1c values that diagnose DM

A

FPG 126+
2-hour 200+ during a 75g Oral glucose tolerance test
A1c 6.5+

217
Q

How does DKA come about?

A

Insulin Deficiency causes FFA release, making ketones
Shock, dehydration release epinephrine
Epi means body cant use glucose, accumulates
Glucagon promotes gluconeogenesis
Kidneys dump glucose, ketones: osmotic diuresis

218
Q

Complications of pheochromocytoma

A

Chronic causes cardiomyopathy

219
Q

Lactotrophic pituitary adenoma presentation

A

F: Amenorrhea, Galactorrhea, low libido, infertility, mass
M: Decreased libido, sperm count, mass effect

220
Q

Hypocalcemia findings

A

Behavioral disturbances, stupor, cramps, convulsions
Trosseau, chovstek signs
Prolonged QT

221
Q

Anaplastic Carcinoma of the thyroid

A

Uncommon, in elderly, highly aggressive
Present with mass effect, die within year of invasion
Microscopy shows papillary CA w/ high grade tumor

222
Q

Definition of short stature

A

Hight 2 SD below mean for age and sex (below 3rd%)

Height more than 2 SD below pid-parental height

223
Q

What ketones accumulate in DKA?

A

Acetoacetic acid

Beta-hydroxybutyrate

224
Q

Precursors to DKA

A

Pneumonia, UTIs

Non-compliance is the most common cause (DMI)

225
Q

How would you identify nephropathy in a patient with DMII?

A

Spot (random) urine sample: urine dipstick not sensitive to proteinuria below 300mg. Most common protein is Albumen

226
Q

Ddx for pediatric tall stature

A

Beckwith-Wiedemann (IGF-2, big head)
Homocystinuria (methionine metabolism error)
Klinefelter (47XXY)
Marfan (Fibrillin-1 mut, Dx by Ghent Nosology)

227
Q

Posterior pituitary hormones

A

ADH (deficient = DI, excess = SIADH) and Oxytocin

228
Q

Lactotroph adenoma histology

A

Stromal hyalinization with Psamomma bodies

Dense calcification

229
Q

Findings of diabetic nephropathy

A

Glomerular sclerosis: thickening of BM, disruption of protein cross-linkages that make barrier, causes large molecule (protein) leak (Kimmelstiel-Wilson Disease)
Renal vascular lesions (arteriolosclerosis)
Pyelonephritis

230
Q

Differentiate corticotroph pituitary adenomas vs ACTH-secreting tumors and adrenal tumors

A

Pituitary Coricotroph: ACTH supression w/ high dose dexamethasone suppression test.
Ectopic corticotroph: Not suppressed, high serum cortisol AND corticotropin
Adrenal tumor/hyperplasia: not suppressed, high cortisol

231
Q

Presentation of regular hyperthyroidism

A

Exopthalmos, Jittery, palpitations, sweating, flushing

232
Q

When can you start intermediate or long-acting insulin in a DKA patient?

A

Mental status and GI issues improve
Anion gap normalized
Allow overlap time of 30-60 min

233
Q

Adverse drug interactions of sulfonylureas

A

Displace from binding w plasma proteins (sulfonamides, clofibrate, salicylates, other NSAIDs)
Ethanol
Inhibiting CYP enzymes (azalea antifungals, gemfibrozil, cimetidine)

234
Q

Progression of Hashimoto thyroiditis

A

Immune mediated insult, then hyperactivity and enlargement, then follicular cell exhaustion

235
Q

When do growth spurts usually occur?

A

First 18 months, when more table food is introduced

Can be catch-up or catch-down

236
Q

Presentation of Glucagonoma

A

Mild diabetes
Characteristic rash: Necrolytic migratory erythema on groin, lower extremities. Progresses to shedding, bull, crusted erosions
4 D’s: Diabetes, Dermatitis, Depression, DVTs

237
Q

Drug targeting factors of insulin secretion regulation

A

Resting membrane potential (specifically Katp channel)
VDCC (L-type Ca channel)
GPCR-Gs / Gi / cAMP axis

238
Q

Treatment for corticotroph pituitary adenomas

A

Somatostatin analogs, bromocriptine, surgery

they can express DA / somatostatin recs

239
Q

Sx of hypoglycemia

A

Confusion, seizures, coma
Sympathetics (tachycardia, palpitations, sweat, tremor)
Parasympathetics: Hunger, nausea
Tx w/ glucose or sucrose or glucagon

240
Q

Major side effects of Methimazole

A

Agranulocytosis, leukopenia, thrombocytopenia, etc
Elevated Serum transaminases, jaundice, hepatitis
Be careful if they have liver disease/EtOH/hepatitis!!

241
Q

Differentiate central vs nephrogenic DI in the clinic

A

Administer DDAVP

Water better retained? Central. No? Nephrogenic

242
Q

Types of amiodarone-induced thyrotoxicosis

A

1: underlying thyroid pathology (like graves)
2: Amiodarone-caused, release pre-formed thyroid hormones into the circulation

243
Q

Amiodarone

A

Commonly Rx for arrhythmia
Can cause Type II amiodarine induced thyrotoxicosis (actual thyroid tissue destruction)
Repeat TSH, free T3/4 levels q6-12mo
Check for emerging sx of hyperthyroidism

244
Q

Congenital Hypoparathyroidism causes

A

DiGeorge: defects in 3rd/4th pharyngeal pouches, parathyroid glands maybe absent or underdeveloped
CASR germline mutations: familial hypocalcemic hypercalciuria (hyperactive Ca-sensing receptors)
Familial isolated Hypoparathyroidism: Precursor PTH cant get all the way to functional PTH

245
Q

Somatotrophin pituitary adenoma

A

Gigantism (before epiphyseal closes), Acromegaly (after)
Serum levels of IGF-1 elevated? oral glucose tolerance test for GH response
Enlarged viscera, fatal CV problems, Joint pain

246
Q

Genetics of papillary carcinoma of the thyroid

A

RET/PTC rearrangements: constitutive TK activity

BRAF GOFs: MAP kinase signaling

247
Q

Medullary thyroid carcinoma

A

Sporadic: Most common, univocal, aggressive, 50y.o.
Familial: 100% 15-year survival, multifocal, 43 y.o.
Ass’d w/ RET oncogene on chr 10

248
Q

Adrenocortical insufficiency gives you a lack of mineralocorticoids. What would this look like?

A

Hyper-K, hypo-Na

249
Q

Most common auto-ab in grave’s

A

Thyroid stimulating hormone receptro antibody

250
Q

Differentiate adenomatous vs carcinomatous adrenal cortical neoplasms

A

both are incidental, functional

Carcinomas compress/invade and virilize

251
Q

What does A1c measure?

A

Glucose binding to RBCs
Gives 3-4 month average of blood sugars
Less than 6.5 is good

252
Q

Most common cause of Cushing sydnrome

A

Iatrogenic: glucocorticoid administration

253
Q

Pleomorphic spindle cells

A

Anaplastic Thyroid CA

ENRP (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions