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NR283/ NR 283 (N EW 2025/ 2026 U PDATE) FINAL EXAM:
PATHOPHYSIOLOGY GUIDE| QUESTIONS & ANSWERS| GRADE A|
100% CORRECT (VERIFIED SOLUTIONS)- CHAMBERLAIN
1. Diabetes insipidus (DI) - ANS ✓-rare
-causes by trauma, tumor on pituitary, craniotomy
-Sx: polyuria (frequent urination) and polydipsia (increases thirst)
-not enough ADH so dumping tons of water into urine, so pt. Is severely
dehydrated. All of the water is exiting through the kidneys and now have an
inability to concentrate urine (ability to pick and choose what we want in the
nephron)
-increased plasma osmolality: blood vessel with not enough water and tons of
solutes, hyperosmolar state, blood is thick and viscous, syrupy due to lots of
solutes
-hypernatremia not related with intake of salt, all a water problem
-Sx: increased thirst due to losing a lot, urinating at night, can lose up to 20 L of
urine in a day (hypovolemic), tachycardic: super dehydrated so heart has to work
harder and there isnt a lot of volume
Tx: vasopressin (artificial ADH)
2. Diabetes - ANS ✓-common
-important to note that insulin is dangerous
-beta cells in pancreas produce insulin
-normally: when there is glucose in the blood, insulin gets released from the beta
cells into the blood stream. Insulin acts a key to get glucose inside the cells.
Insulin is water soluble so it needs a second messenger to take it to the nucleus.
-hyperglycemia: tons of sugar in blood
-type 1: dont make enough insulin
-type 2: insulin resistant, down regulation
-Diagnose: hemoglobin A1C or hba1c - draw blood and look at RBC's, look at how
blood sugar levels have fluctuated in the last 3 months, want this to be below 7.
3. Type 1 Diabetes - ANS ✓-insulin deficient
-hypoglycemia that is caused by autoimmune
-childhood disease
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-For some reason our body produces AB's that attack pancreas and we stop
making insulin. We become deficient, lose ability for beta cells to pump out
insulin. If we don't have insulin we end up with tons of glucose molecules in
blood stream and none of it is making it into cells
-RF: family history, environment, asians, african americans
Sx: 3 p's, weight loss initially since sugar is not entering into cells, starving,
fatigue (no ATP), increased infection (bugs love sugar), rapid onset.
-will need external insulin forever
4. 3 P's of diabetes - ANS ✓-polyuria: increased urination due to body trying
to get rid of excess sugar, kidneys are helping out, trying to get rid of sugar
molecules, but its not a good thing for glucose to up in urine and nephron
(indicator that something is off)
-polyphagia: increased hunger - glucose is not making its way into cells, staying
in blood stream so cells are starving
-polydipsia: increased thirst - a lot of solutes in blood (syrup blood), brain is
going to increase thirst mechanism to try and balance osmolality of the blood,
also due to increased urination
5. Type II Diabetes - ANS ✓-problem is insulin resistance, pancreas is
pumping out so much insulin to make up for tons of glucose and cells are
super tired of seeing insulin, cells become insulin resistant
-RF: lifestyle related, obesity, age, HTN (blood moving to quickly, epithelial injury
damage - glucose damaging to body because all of the complications that come
from diabetes are from how damaging this molecule is, as glucose is rocketing
through a blood vessel at a fast rate and it stabs the side of a blood vessel and
causes damage and can start atherosclerosis, also has issues getting through
kidneys and tiny arteries
-decreased insulin secretion: diabetes is a progressive problem - can move
forwards or backwards
-Tx: strict diet or oral medication: glycerides, metformin (helps pancreas to
produce more insulin or on cells themselves to be become more receptive - can
still move backwards and cure yourself of diabetes)
-once you become insulin dependent and cant go backwards and need insulin for
life, pancreas has quit and pancreas does not work anymore so resembles type 1.
Sx: 3 p's decreased energy, obese, recurrent infections (bacteria loves sugar), FBS
is greater than 125 mg/dl
6. Acute complications of diabetes - ANS ✓-Slightly incorrect dose of
insulin can drop blood sugar so low so they can slip into a coma and die
(hypoglycemia) - insulin shock - too much insulin, rapid onset (sweaty,
irritability, confusion, seizures, coma)
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-Diabetic ketoacidosis: crazy high blood sugar (600, 700)
-Occurs from too little insulin and body is starving and we go into backup
metabolism - break down fats and proteins and get ketones. Ketones are
extremely acidic cant live on this alone. When we get super high levels of ketones
then you end up in metabolic acidosis - DKA is most common cause. Body
compensates by respiratory system - deep, rapid respiration (kussmaul
respirations) using accessory muscles to blow of CO2, sweet smelling breath or
urine or sweat from ketones (acetone production which is super sweet), will all
this acidity you have CNS depression
-Causes: type 1 diabetic about to be diagnosed (come into ED lifeless - cells have
been starving for so long, so body has to do backup metabolism, type 2 that
doesn't follow diabetic diet, diabetics who are sick (vomiting, flu) - so don't take
insulin. Metabolic needs change when you are sick.
7. Chronic complications of diabetes - ANS ✓• Acute retinopathy
• Diabetic nephropathy
• Neuropathy:
• Nerves are not functioning anymore (cut off or eaten away)
○ Tends to happen first in feet and hands (numbness and tingling sensation)
• Danger: don't inspect feet often, can step on something and they don't feel it,
bugs love sugar so they can get an infection, an ulcer, can get gangrene - end up
with amputations
• Heart attack: all due to atherosclerosis due to so much glucose (throwing stars)
• Stroke: atherosclerosis
• Peripheral vascular disease: atherosclerosis
• Glaucoma/cataracts: tiny vessels behind eyes can get clogged and damaged
• Infection
8. Nephron - ANS ✓-putting things in and out of fridge:
- Put everything into glomerulus, then everything gets thrown into nephron with
the exception of large molecules that should into go into nephron (blood and
albumin) - too large and damage glomerulus. Everything gets pumped into
glomerulus and goes into nephron as filtrate. First function is filtration. Can
manage ability to pull things into nephron (glomerular filtration rate GFR).
Proximal tubule: sodium, potassium, water, take everything out of fridge. Next go
to reabsorption - hey I actually want to keep some of that potassium and sodium,
putting things back into fridge, starts in proximal tubule and finished up in loop
of Henle. Loop of Henle is water reabsorption and does it passively - osmosis.
Distal tubule: third function: secretion, bodies last effort to get rid of toxins,
deposit urea into collecting duct - active process - active transport - ATP. ADH
acts on distal tubule and collecting duct - last say on how much water we want to
keep. Whatever is left after this process makes urine
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