NRS 313 Study Guide - Final Guide: Muscle Weakness, Hyperkalemia, Heat Intolerance

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Internal Regulation/ Hormones
Fluid balance and sepsis:
o Periorbital swelling: generated systemic swelling.
o Liver disease: infection (sepsis) or anaphylaxis occurs
We get lower production of Serum Albumin
o Inflammation Lab tests
Complement system = Opsinin (measured by CRP)
Kinin System = Bradykinin (vasodilator)
Clotting = ESR, Fibrinogen, Platelets
CBC w/ differential (Measures WBC RBC)
Serum Albumin
K+
Blood culture (sepsis)
Nitrates
Urinalysis
Specific gravity >1.030
Proteinuria
Procalcitonin: levels of bacteria
Syndrome of inappropriate (EXCESSIVE) Antidiuretic hormone
o causes generalized swelling
o Realses ADH even if we don’t need it
o Comes from the pituitary
o Can be caused by head trauma, cerebral hematomas, cerebral vascular accident
o Kidney retains H20 back into vascular space
o Sx
Tachycardia
Bounding pulse
Hypertension
Decrease in Hemeglobin
Decrease in urinary output (oliguria)
Decrease in hematacrit
Weight gain
Decrease in Na+
o Oliguria = <30ml/hr
o Polyuria = 2000ml/day (or 83ml/hr)
Mechanisms of Hormonal Alterations
o Inappropriate amounts (Not enough, or too much) of hormone delivered to the
target cell
inadequate hormone synthesis / production
Example: Type one diabetes
o Inappropriate response by the target cell
cell surface receptor-associated disorders
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Intracellular function disorders ROS
Example: Insulin resistance (Type 2). Resistin created by the breakdown
of adipocytes. Susceptible population: BMI >30. Associated with 85% of
the population living with diabetes
Example: Inappropriate amount (type 1 diabetes)
Too little or too much
(Insulin Deficiency)
15% of all diabetes
Pancreas
o Two main functions
Endocrine: produces hormones.
insulin (beta cells)
glucagon (alpha cells): targets cells in the liver to release glycogen
Exocrine: produces digestive enzymes
Lipase: fats
Trypsin: proteins
Amylase: Carbs
Diabetes
o Types of DM
Type I (beta cell destruction)
Type II (insulin resistance recall the role of resistin)
Diagnosis is based on HbA1c levels (normal range is 3.2 to 6.8%), fasting
plasma glucose, 2-hour glucose tolerance test.
o HBA1C= Hemeglobin A1C= measures hemoglobin over RBSs life
90-120 days. Glucose can become permanently bound to hemoglobin.
Shows how controlled their blood sugar is over months
Not a one time diagnosis
o Insulin Independent review
Cells affected in Retina, Peripheral nerve cells (Schwann) and endothelial
cells
AGEs => ROS => decrease in NO => stiff noncompliant =>
hypertension
Readily gains entry through GLUT Channels
Insulin insufficiency: DKA = Diabetic Ketoacidosis
o Clinical criteria: normal is 70-110
Blood glucose level > 250 mg/dl
Serum pH <7.30
Positive Urine Ketones (lipolysis = fatty acid breakdown = acidic systemic
pH)
PREFERENCE OF BREAKDOWNS
Readily available glucose source
Fats
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Document Summary

Intracellular function disorders ros: example: insulin resistance (type 2). Deep and rapid breathes: cns depression & confusion (r/t acidosis, muscle weakness, lack of energy. Cells need o2 + glucose: thirst, polyuria, dehydration, type 1 or 2, formation of ketone bodies, lypolysis=breakdown of fat-fattyacids get breakdown into ketones. Measured in the urine: proteinlysis= sweet and salty breathe. Aldosterone regulation of potassium and sodium, and water balance: excess aldosterone: water retention and na+ retention deficient. Aldosterone: leads to hyperkalemia: heart dysrhythmias, cortisol glucocorticoid. Impaired gluconeogenesis: symptoms: dehydration, hypoglycemia, hyperpigmentation from increased. T his doesn"t create any sickness however: posteral hypotension: significant drop in bp and rise in hr. lack of. Infertility caused by decreased lh: increased aldosterone, na+ retention and h20 retention. Increases gi motility: growth and maturation of tissue, muscle function and tone. Depleted th causes weakness: high metabolism=hot temperature. Lots of 02 needed: low metabolism= cold temperature, t3= thyroxine: attaches to muscle activated cells.

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