Pituitary Gland Pathology Dr. Singh

Question 1

1. Alpha cells
2. Beta cells
3. Delta cells
4. Acinar cells + duct cells
5. PP cells
6. D1 cells

Answer 1

1. Alpha cells = glucagon
2. Beta cells = Insulin
3. Delta cells = Somatostatin
4. Acinar cells + duct cells = Exocrine pancreas
5. PP cells = Pancreatic polypeptides
6. D1 cells = VIP (Vasoacive GI polypeptide)

Question 2

Insulin given exogenously and insulin made by body have what difference

Answer 2

Insulin made by body has C-peptide on it

Question 3

Insulin main purpose

Answer 3

Give cells food and glucose it needs

Question 4

What happens when you eat food that causes insulin to be secreted

Answer 4

1. Oral glucose = RELEASE INCRETINS ( GLP1 + GIP)
2. GIP And GLP1 release insulin + inhibit glucagon = lowering Blood glucose
3. DPP-4 inactivated Incretins

Question 5

1. T1D

2. T2D

Answer 5

1. T-cell autoimmune attacking Beta- cells, inflammation , circulating auto-ABs
2. Insulin resistance , amyloid deposition

Question 6

When do you show T1D sx

Answer 6

When 90% or more of islets are destroyed (T-cells attack islets beta cells and ones they have been insulted ones then causes autoimmune phenomena)

Question 7

T1D stage 1, 2, 3

Answer 7

1. Autoimmunity, AB there, no functional problems, to sx
2. Autoimmunity + Dyglycemia (how glucose) no SX
3. Autoimmunity + hyperglycemia + SX

Question 8

Major cause of T2D and reason for this

Answer 8

OBESITY
1. Adipokines = accumulate depending on how much adipose , disrupt intracellular pathway enabling insulin uptake
2. FFAs
3. Inflammation = damage Beta cells
(Initially beta cells increase insulin compensation = no sx, when beta cells cant keep up anymore you get DM)

Question 9

T2D must have 1 thing to be DM

Answer 9

Beta cell exhaustion causing Beta Cell Dysfunction

Question 10

Maturity Onset DM of the Young (MODY)

1. What
2. SX
3. Genetic

Answer 10

1. Hybrid between T1D and T2D and usually earlier presentation
2. T2D clinical sx however in young pts, INSULIN can be high low normal, NO Abs, NO ketogenic
3. MODY mutation = loss of glucokinase (what lets glucose enter Beta cells to let them know to secrete insulin)

Question 11

DM and pregnancy, Gestational DM

1. Can happen from
2. Risks

Answer 11

1. Hormones and stress that gives SM clinical symptoms

2. Macrosomic, congenital malformations, Neonatal hypoglycemia* —> Seizures —> Brain damage

Question 12

T1D and T2D SX usually seen

Answer 12

1. T1D : TRIAD : Polyphagia, Polyuria, Polydipsia (4 Ts, Toilet, Thirsty, Tired, Thinner)
   + severe Diabetic Ketoacidosis DKA
2. T2D : fatigue, vision changes

Question 13

T1D DX

Answer 13

1. Auto-ABs seen more in Caucasian only
2. HLA on Chr 6
3. Thin emancipated child

Question 14

DKA TRIAD

Answer 14

1. Hyperglycemia
2. Ketonemia
3. Metabolic Acidosis
   = initial presentation in 20% - 40% T1D

Question 15

DKA can be seen when in T1D

Answer 15

1. Non-compliance
2. Pneumonia
3. UTI
   (Illness, infection = releases epinephrine which causes glucose to be released and kept in blood, insulin deficiency causes FFAs release causing ketones in kidney = dumping ketones + glucose + water = dehydration and shock = more epinephrine released (osmotic diuretics shock)

Question 16

DKA DX

Answer 16

Ketones in urine

Question 17

DKA causing polyuria (from hyperglycemia) + Polydypsia ( from ketonemia) + Ketonuria (from Acidosis) causes what SX

Answer 17

1. Dehydration
2. Tachy
3. Kussmaul Respiration (increase breathing to release more CO2) BLOW OFF

Question 18

Hyperglycemic Hyperosmotic Syndrome (HHS) :

1. What is this
2. SX

Answer 18

1. ACUTE hyperglycemic crisis in T2D, higher gluconeogenesis, low glucose uptake in cells (FROM PROLONG INSULIN DEFICIENCY) = metabolic alkalosis,
2. Glucose over 600 + dehydration
   + Severe dehydration
   + Hyperosmolality (>350) —> coma, altered mental status
   + Impaired renal function

Question 19

Chronic Hyperglycemia risks

Answer 19

1. Stroke
2. MI * most common cause of death
3. Lower Extremity gangrene

Question 20

Glucose accumulation in BVs cause what

Answer 20

Advanced Glycated End Products (AGEs) that combine with proteins causing Cellular Dysfunction and Damage = endothelial dysfunction

Question 21

Diabetic Nephropathy can cause what 3 things

Answer 21

1. Glomerular Sclerosis (thickened BM, disrupt filter, proteinuria)
2. Renal Vascular Lesions (Arterioloscelrosis)
3. Pyelonephritis

Question 22

Diabetic Nephropathy

1. Best stain in early stage and what you see
2. Other stain and way to look at it

Answer 22

1. Electron microscopy : early BM thickening
2. Thickened tubular BM, with PAS stain on Light microscopy
   = thick BM causes more holes and albumin to leak

Question 23

Diabetic Nephropathy effects Glomeruli how 2 ways

Answer 23

1. Matrix accumulation = nodular matrix = PAS+ stain shows you this
   = Kimmelsteil Wilson Disease (nodules in mesangial matrix)
2. Diffuse Nephrosclerosis (nodules grow + contract glomerulus down causing diffuse sclerosis)

Question 24

Diabetic Nephropathy DX

Answer 24

Microalbuminuria in Urine Albumin Testing (even a small amount of albumin)

Question 25

Normal to diabetic retinopathy what happens

Answer 25

1. Neovascularization (hypoxia —> VEGF = not well made BVs——>, hemorrhage, blindness) ** 2. Other things : glaucoma, cataracts (Cotton wool patches= places of ischemia and infarction in retina)

Question 26

ANS neuropathy condition in DM

Answer 26

ANS neuropathy can cause silent MI with just N,V (later can cause CP_)

Question 27

Pancreatic Neuroendocrine Tumor (PanNET) 1. Looks like + location 2. Histo

Answer 27

1. Solid, tan, yellow on islets of the neck and tail | 2. well-differentiated neuroendocrine tumor + secretory granules (salt and pepper chromatin)

Question 28

GET NET

Answer 28

Gastroenteropancreatic Neuroendocrine tumor ( similar to PanNET)

Question 29

Insulinoma : 1. Cell involved and clinical feature 2. B/M 3. Histo 4. Lab to do

Answer 29

1. B cell, hypoglycemia (under 50) 2. Benign 3. Small , Amyloid found 4. Check C-peptide amount on insulin (if there is a lot of C-Peptide then + , if not then they are taking in too much insulin)

Question 30

Gastrinoma 1. Cell involved and clinical feature 2. Triad of the syndrome it causes

Answer 30

1. G cell, Zollinger Ellison Syndrome (secretes Gastrin) | 2. Islet cell tumor, Gastric Acid Hypersecretion, Peptic DUODENAL Ulceration (not responding to tx)

Question 31

Somatostatinoma 1. Cell involved and clinical feature 2. M/B 3. What it causes 4. SX 3 main ones

Answer 31

1. Gamma cell , Gallstones, pancreatic head 2. Very metastatic 3. Sshes cells around it (Insulin B-cells esp, + lower gallbladder motility, + lower exocrine pancreatic secretions = malabsorption) 4. DM symptoms (hard to dx), cholelithiasis, steatorrhea

Question 32

Glucagonoma 1. Cell involved and clinical feature 2. SX (Quad Ds) 3. Skin sx

Answer 32

1. Alpha cell, Hyprglycemia, rash 2. DM mild + Dermatitis, + Depression + DVTs 3. Necrolytic migratory erythema rash (groin + lower extremities)

Question 33

VIPoma 1. Cell involved and clinical feature 2. B/M 3. Causes what 4. SX

Answer 33

1. D1 cell, WDHA syndrome 2. Very metastatic 3. Secretes Vasoactive Intestinal Peptide 4. Watery diarrhea, Hypokalemia, Achlorhydria (+ 20% have flushing also = mimin carcinoid tumor)

Question 34

Adolescent male with ABD pain, CT shows free air in abd, + a perforated gastric ulcer

Answer 34

Pancreatic mass, Gastrinoma