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ENRP Exam 2 > Pituitary Gland Pathology Dr. Singh > Flashcards

Pituitary Gland Pathology Dr. Singh Flashcards

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

Insulin given exogenously and insulin made by body have what difference

A

Insulin made by body has C-peptide on it

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3
Q

Insulin main purpose

A

Give cells food and glucose it needs

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4
Q

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

A
  1. Oral glucose = RELEASE INCRETINS ( GLP1 + GIP)
  2. GIP And GLP1 release insulin + inhibit glucagon = lowering Blood glucose
  3. DPP-4 inactivated Incretins
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5
Q
  1. T1D

2. T2D

A
  1. T-cell autoimmune attacking Beta- cells, inflammation , circulating auto-ABs
  2. Insulin resistance , amyloid deposition
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6
Q

When do you show T1D sx

A

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)

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7
Q

T1D stage 1, 2, 3

A
  1. Autoimmunity, AB there, no functional problems, to sx
  2. Autoimmunity + Dyglycemia (how glucose) no SX
  3. Autoimmunity + hyperglycemia + SX
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8
Q

Major cause of T2D and reason for this

A

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)

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9
Q

T2D must have 1 thing to be DM

A

Beta cell exhaustion causing Beta Cell Dysfunction

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10
Q

Maturity Onset DM of the Young (MODY)

  1. What
  2. SX
  3. Genetic
A
  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)
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11
Q

DM and pregnancy, Gestational DM

  1. Can happen from
  2. Risks
A
  1. Hormones and stress that gives SM clinical symptoms

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

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12
Q

T1D and T2D SX usually seen

A
  1. T1D : TRIAD : Polyphagia, Polyuria, Polydipsia (4 Ts, Toilet, Thirsty, Tired, Thinner)
    + severe Diabetic Ketoacidosis DKA
  2. T2D : fatigue, vision changes
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13
Q

T1D DX

A
  1. Auto-ABs seen more in Caucasian only
  2. HLA on Chr 6
  3. Thin emancipated child
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14
Q

DKA TRIAD

A
  1. Hyperglycemia
  2. Ketonemia
  3. Metabolic Acidosis
    = initial presentation in 20% - 40% T1D
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15
Q

DKA can be seen when in T1D

A
  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)
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16
Q

DKA DX

A

Ketones in urine

17
Q

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

A
  1. Dehydration
  2. Tachy
  3. Kussmaul Respiration (increase breathing to release more CO2) BLOW OFF
18
Q

Hyperglycemic Hyperosmotic Syndrome (HHS) :

  1. What is this
  2. SX
A
  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
19
Q

Chronic Hyperglycemia risks

A
  1. Stroke
  2. MI * most common cause of death
  3. Lower Extremity gangrene
20
Q

Glucose accumulation in BVs cause what

A

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

21
Q

Diabetic Nephropathy can cause what 3 things

A
  1. Glomerular Sclerosis (thickened BM, disrupt filter, proteinuria)
  2. Renal Vascular Lesions (Arterioloscelrosis)
  3. Pyelonephritis
22
Q

Diabetic Nephropathy

  1. Best stain in early stage and what you see
  2. Other stain and way to look at it
A
  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
23
Q

Diabetic Nephropathy effects Glomeruli how 2 ways

A
  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)
24
Q

Diabetic Nephropathy DX

A

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

25
Q

Normal to diabetic retinopathy what happens

A
  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)

26
Q

ANS neuropathy condition in DM

A

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

27
Q

Pancreatic Neuroendocrine Tumor (PanNET)

  1. Looks like + location
  2. Histo
A
  1. Solid, tan, yellow on islets of the neck and tail

2. well-differentiated neuroendocrine tumor + secretory granules (salt and pepper chromatin)

28
Q

GET NET

A

Gastroenteropancreatic Neuroendocrine tumor ( similar to PanNET)

29
Q

Insulinoma :

  1. Cell involved and clinical feature
  2. B/M
  3. Histo
  4. Lab to do
A
  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)
30
Q

Gastrinoma

  1. Cell involved and clinical feature
  2. Triad of the syndrome it causes
A
  1. G cell, Zollinger Ellison Syndrome (secretes Gastrin)

2. Islet cell tumor, Gastric Acid Hypersecretion, Peptic DUODENAL Ulceration (not responding to tx)

31
Q

Somatostatinoma

  1. Cell involved and clinical feature
  2. M/B
  3. What it causes
  4. SX 3 main ones
A
  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
32
Q

Glucagonoma

  1. Cell involved and clinical feature
  2. SX (Quad Ds)
  3. Skin sx
A
  1. Alpha cell, Hyprglycemia, rash
  2. DM mild + Dermatitis, + Depression + DVTs
  3. Necrolytic migratory erythema rash (groin + lower extremities)
33
Q

VIPoma

  1. Cell involved and clinical feature
  2. B/M
  3. Causes what
  4. SX
A
  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)
34
Q

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

A

Pancreatic mass, Gastrinoma

ENRP Exam 2 (8 decks)

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