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Z - M2 Endo/Repro > Endocrine - Pathology > Flashcards

Endocrine - Pathology Flashcards

1
Q

Insulin Physiology - Transports (4)

A

GLUT-4 - Insulin Dependent - Skeletal Muscle/Adipose + Increase glucose uptake with insulin via lipogenesis + potein synthesis + glycogen synthesis

GLUT-1 (Brain/RBC/Eye) - Non-Insulin Dependent
GLUT-2 (B-Cells + Liver) - Non-Insulin Dependent
GLUT-3 (Brain) - Non-Insulin Dependent

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2
Q

Type I vs. Type II DM - Histology

A

Type 1 - Islets with lymphocytic infilitrate

Type II - Islets with amyloid depostion + kidney with hyaline arteriosclerosis + Kimmelstiel-Wilson Nodules

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3
Q

Type I DM Genetics

A

Not Strong Genetic Link - HLA-DR3/4

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4
Q

MEN 1 - 3 Diseases + Genetics

A

Parathyroid Hyperplasia/Tumor

PEN - Pancreatic Endocrine Tumor (Insulinoma)

Pituitary Adenoma

MEN1 Tumor Supressor Gene Knockout

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5
Q

MEN 2A/2B - 3 Diseases + Genetics

A

2A
Medullary Thyroid Cancer
Pheocromocytoma
Parathyroid Hyperplasia

2B
Medullary Thyroid Cancer
Pheocromocytoma
Ganglioneuromas of mucosal sites

RET Oncogene Mutation

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6
Q

Insulinoma - Key Findings (3)

A

1) Eposodic hypoglycemia episodes (confusion/stupor/LOC)
2) Histology shows amyloid deposition
3) Increased C-Peptide

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7
Q

Signs/Symptoms of Hypoglycemia (6)

A

1) Neurogenic - Excess Epi/NE

Neuroglycopenic

1) Blurred Vision
2) Confusion
3) Aggression
4) Seizures
5) Memory Loss

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8
Q

Common Causes of Hypoglycemia

A

1) Facticious
2) Insulinoma
3) Excess Diarrhea (no absorption)
4) Ketoisic (active child uses up all their glycogen)
5) Alcoholic Induced
6) GIST Tumor Producing IFG-1

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9
Q

Hypoglycemia Causing Drugs (3)

A

1) Diabetes Tx
2) Alcohol
3) Sulfonamide Antibiotics

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10
Q

General Rules of Endocrine Testing (2)

A

1) Hyposecretion - Stimulation Test - Missing Cortisol? Run stimulation test to see if ACTH increases it or not (if yes then the issue is low ACTH production, if no then the adrenal isn’t responding to the ACTH = Primary)
2) Hypersecretion - Suppression Test - E.g. give dexamathsone overnight - Should result in less morning ACTH (since coritsol is elevated all night) - No suppression = ACTH secreting tumor = Secondary

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11
Q

Prolactinoma - Findings (4)

A

1) Increased Prolactin + Decreased FSH/LH
2) Galactoria
3) Amenorrhea
4) Male loss of libido

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12
Q

GH Adenoma - Key Findings (2)

A

1) Secondary diabetes via GH/IGF-1

2) Often with co-secretion of prolactin (glactoria)

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13
Q

Sheehan Syndrome - Pathophysiology + Presentation (3)

A

Increased hormone demand of pregnancy - leads to enlargement of the Pituitary - Blood loss in birthing triggers infarction of the pituitary

Presentation

1) Poor Lactation
2) Loss of Pubic Hair
3) Fatigue in Postpartum Stage

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14
Q

Kallman’s Syndrome - Pathophyisology

A

Failure of GnRH cells to migrate from olfactory region - Anosmia + failure of GnRH to develop (low FSH/LH)

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15
Q

Cortisol Testing - Most Sensitive + Most Specific

A

Most Sensitive - 24 Hour Free Cortisol

More Specific - Low Dose Dexy Test

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16
Q

Adrenal Cortex Layers (3)

A

GFR + Salt, Sugar, Sex
Glomerulosa = Mineralcorticoids
Fasicular = Glucocorticoids
Reticularis = Androgens

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17
Q

Signs/Symptoms of High Cortisol (9)

A

1) Hyperglycemia/DM
2) HTN (Increased A1 Receptros from Epi)
3) Moon Facies
4) Central Obesity
5) Violaceous Straie
6) Menstrual Irregularities
7) Osteoporosis
8) Muscle Wasting/Weakness
9) Immune Suppression

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18
Q

Pathophysiology of Glucocorticoid Immune Suppresion (3)

A

1) Inhibit Phospholipase A2 - No Arachodonic Acid Metabolites (E.g. PGE2)
2) Inhibit IL-2 (T-Cell Growth)
3) Decreased Mast Cell Degranlation

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19
Q

CT Differential of Cushings

A

Primary Disease = Unilateral hypertrophy + atrophy of contralateral
Secondary Disease = Bilateral hyperplasia

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20
Q

Primary Mineral Corticoid Excess - Name + MCC (2) + Presenting S/Sx (5)

A

Conn Syndrome

Bilateral Adrenal Hyperplasia = Adolsterone Secreting Adenoma

S/Sx

1) High Aldosterone
2) HTN
3) Hypernatremia
4) Hypokalemia
5) Metabolic Alkalosis

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21
Q

Signs/Symptoms of Primary Adrenal Insufficiency (6)

A

1) Hypotension (Low Cortisol)
2) Weakness (Low Cortisol
3) Weight Loss (Low Cortisol
4) Hyperkalemia (Low Aldosterone)
5) Metabolic Acidosis (Low Aldosterone)
6) Hyperpigmentation (High ACTH)

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22
Q

Pheochromocytoma - S/Sx (5) + Diagnosis

A

1) Pressure (HTN)
2) Pain (Headache)
3) Perspiration
4) Palpitation
5) Paroxysmal (On/Off for 20 minutes)

Urine Metanephrines + Vaillymandelic Acid

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23
Q

Pheochromocytoma - Treatment

A

Step 1 - 1-2 Weeks Prior - Alpha Block (Phenoxybenzamine + Prazosin)
Step 2 - 2-3 Days Prior - Beta Block (Propranolol + Atenolol)

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24
Q

Adrenocortical Carcinoma - Classic Presentation + S/Sx (3)

A

Female with rapid onset oily skin + hirtuism from excess andersteindione

1) Mass Effect (Abdominal Pain
2) Metastasis
3) Rapid Onset hormone secretion (any layer)

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25
Q

Congenital Adrenal Hyperplasia - Pathophysiology + Genetics + Types (2)

A

Missing steroidogenesis enzyme - Results in deficiencies + bilateral adrenal hyperplasia

Autosomal Recessive
21-Oh Deficiency - No MC/GC + Excess Sex Steroids
17-Oh Deficiency - No GC/Sex with Excess Aldosterone

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26
Q

21-Hydroxylase Deficiency - Key Findings (6)

A

1) High Sex Steroids
2) Hypotension
3) Hyperkalemia (Low Alodosteone)
4) Addison’s S/Sx
5) Big Penis (Male) + Ambiguous Genitalia (Female)
6) 17-OH Build Up

27
Q

17-Hydroxylase Deficiency - Key Findings (3)

A

1) Low Cortisol + Sex Steroids
2) HTN (High Aldosterone)
3) Hypokalemia (High Aldosterone)

28
Q

Hashimoto’s Thyroiditis - Pathophysiology

A

Auto-immuno destruction of TPO - Produces iodized TH - Loss leads to hypothyroid
Associated with lymphocytic infiltration and the HLA-DR5 subtype which causes CD8 mediated cell death

29
Q

Drugs Inducing Hypothyroid (3)

A

1) Amiodorone
2) Lithum
3) Iodide Dyes

30
Q

Hypothyroid S/Sx (7)

A

1) Intolerance to cold
2) Fatigue Weakness
3) Modest weight gain
4) Loss of lateral eyebrows
5) Dry brittle hair/nails
6) Hypercholesterolemia
7) Constipation

31
Q

Hashimoto’s Exam Findings (1) + Histology (2) + Extra S/Sx

A

Moderatly enlarged non-tender thyroid

Hurthle cells + lymphoid aggregates with germinal centers (increased B-Cell Lymphoma Risk)

Increased TSH Response = Increased Prolactin = Galacturia + Amenoreahhea

32
Q

Thyrotoxicosis - Signs/Symptoms (7)

A

1) Anxiety
2) Increased NE/Epi Signs
3) Heat Intolerance
4) Increased Bowel Movement
5) Hyper-reflexive
6) Increased A-Fib
7) Bone resportion with hypercalcemia

33
Q

Graves Disease - Signs/Symptoms (4)

A

1) Normal Hyperthyroid (anxiety, heat intolerance etc.)
2) Pretibial myxedema (edema via glycosaminoglycans)
3) Opthalmopathy
4) Scalloping of follicle on histolgoy

34
Q

Graves Disease - Pathophysiology

A

Ab (IgG) that stimulates the TSH Receptor (Thyroid Stimulating Antibody = TSI)

35
Q

Multinodular Goiter - Pathophysilogy

A

Heterogenous follicles - Hot (active) + cold (possibly malignant) - Focal patches operate independent of TSH = hyperthyroid

36
Q

Goiter Classification - Use TSH

A

Low TSH (Thyrotoxic) - Diffuse = Goiter vs. Irregular = Multinodular

Hypothyroid - Iodine Deficiency of Hashimoto’s

Euthyroid - Iodine Deficiency + Solitary Nodule (Adenoma, Cyst, Cancer) – Check Calcatonin (Elevated = Medullary)

37
Q

Radioactive Iodine Test - Hot vs. Cold

A 
Hot = Graves or Goiter
Cold = Limited Uptake = Adenoma or Carcinoma
38
Q

Papillary Thyroid Cancer - Key Points (4) + Histology

A

1) Most common thyroid cancer
2) Age 25-50
3) Good Prognosis
4) Associated with radiation exposure (E.g. Hodgkin’s Tx or Radioactive Disaster)

Histology = Psammoma bodies + finger like projectsion with ground glass nuclei (orphan annie cells)

39
Q

Follicular Thyroid Cancer - Key Points (4) + Histology

A

1) Most common in areas of iodine deficiency
2) Tyrosine Kinase gain of function
3) Hematogenous spread (not normal for carcinoma)
4) Peak Age = 40-60

Malignant proliferation through the follicle and into the basement membrane

40
Q

Anaplastic Thyroid Cancer - Key Points (3) + Histology

A

1) Poor Prognosis
2) Painful (like subacute thyroiditis)
3) Dysphagia common

Histology
Highly invasive dysmorphic cells

41
Q

Medullary Thyroid Cancer - Key Points (4) + Histology

A

1) C-Cell Proliferation (Calcatonin Production)
2) RET Mutation (MENA/B) + Familial (Later Onset)
3) Calcitonin lowers serum calcium levels

Histology
Hylanizng amyloid stroma with polygonal cells in nest + apple green biferingence on congo-red staining

42
Q

Levothyroxine - Dosing + Toxicities (3)

A

Dose 30 Minutes Before Meal, Iron, Soy, Ca all interfere with absorption

1) TSH Suppression causes cardiotoxic affects (A-Fib)
2) Overdose Risk
3) Allergic Reaction

43
Q

Propythiouracil - Use + Mechanism + Toxicity (3)

A

PTU = Anti-Thyroid - Used for 1st 3 Months of Pregancy

Mechanism - Inhibits T4-T3 Conversion

Toxicity - Liver Failure + Agranulocytosis + Rash

44
Q

Methamazole - Use + Mechanism + Toxicity (3)

A

MMI = Anti-Thyroid for any time but 1st Trimester

Mechanism - Inhibits TPO

Toxicity - Less Liver Failure (vs. TPU) + Agranulocytosis + Rash

45
Q

Constitutional Growth Delay - Key Points (3)

A

1) Normal “Late Bloomer)
2) Delayed Puberty + Bone Age
3) Will Reach Target Height (Mid-Parental)

46
Q

Dysmorphic Causes of Short Stature (3)

A

1) Turner’s
2) Trisomy 21
3) DiGeorge

47
Q

Turner’s Syndrome - Key Findings (5) + Genetics

A

Loss of part of an X Chromosome

Findings

1) Webbed Feet
2) Floppy Skin
3) Shortened IVth Metacarpal
4) Coartation of the Aorta
5) Hashimoto’s

48
Q

Non-Dysmorphic Causes of Short Statue (5)

A

Normal Weight

1) Chronic Illness
2) Eating Disorder

Increased Weight

1) GH Deficiency
2) Hypothyroidism
3) Cushing

49
Q

Congenital GH Deficiency S/Sx (3)

A

1) Micropenis
2) Hypoglycemia
3) Look younger than natural age

50
Q

GH Treatment - Side Effects (4)

A

1) Pseudotumor
2) Hyperglycemia
3) Thyroid Dysfunction
4) Malignancy

51
Q

Tall Stature - Causes - (5)

A

1) GH Excess (MEN1 = Pituitary Adenoma)
2) GH Excess (McCune Albright Syndrome)

3) Genetics - Klinefleter
4) Genetics - Marfan
5) Genetics Homocytinuria

52
Q

McCune Albright Snydrome - S/Sx (3)

A

1) Precocious Puberty

2) Cafe-Au-Lait- Macules + Increased Gs Activity

53
Q

Klinefelter Syndrome - Key Points (4)

A

1) XXY
2) Gynecomastia
3) Small Testes + Absent Spermatogenesis
4) Tall Stature

54
Q

Premature Adrenarch - Subpopulation + Predisopistion

A

Black Girl - PCOS Risk

55
Q

Familial Male Limited Precocious Puberty - Key Points (3)

A

1) LH Receptor Mutation causes precocious puberty
2) Autosomal dominant + Male
3) Premature leydig cell maturation with small testes

56
Q

Hypthalamic Hamartoma - Key Points (2)

A

1) Benign tumor causing precocious puberty

2) Gelastic Seizures (laughing seizures)

57
Q

Hyperthyroid Impact on Testosterone

A

Increases SBHG = Less Free Testosterone

58
Q

5-Alpha-Reductase - Function + Key Role

A

Converts Testosterone to Dihydrotestosterone

DIT = Key for External Genital = Pubic Hair Growth in Male + BPH

59
Q

DDx of Low Serum Testosterone - Next Step + Differential by 2 Groups

A

Check LH/FSH

Elevated = Karotype Issue (Primary Gonad Issue) = Klinefelter’s

Low = Secondary = Measure Prolactin + Pituitary Functino

60
Q

Klinefelter’s - Key Feautures (4)

A

1) XXY
2) Genetically Male with Less Puberty Development
3) Gynecomastia
4) Low Testosterone + High FSH/LH

61
Q

Kallman’s Syndrome - Key Features (5)

A

1) Low GnRH + FSH/LH
2) Due to Olfactory Migration Issue
3) Anosmia
4) AD or AR
5) Pubic Hair Still Present (No Adrenal Androgen Production Inhibition)

62
Q

Complete Androgen Insensitivity - Key Features (3)

A

1) Male’s present as females with normal appearing breasts + female genitalia
2) High Testosterone trying to activate insensitive receptors

63
Q

5-Alpha Reducatase Deficiency - Key Features (4)

A

1) Bifid Scrotum
2) Hypospadias
3) Variable Childhood Phenotype
4) Virilization at puberty

Z - M2 Endo/Repro (3 decks)

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