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110 Cards in this Set

  • Front
  • Back

CATIONS

Positively Charged Molecules


(Na+, K+, Ca+, Mg+)

ANIONS

Negatively Charged Molecules


(HCO3-, Cl-)

SERUM OSMOLALITY NORMAL

275-295mOsm/kg


(300-900 urine)

ANTICOAGULANTS

Sodium EDTA, Sodium Heparin, Sodium Citrate


(Bad for electrolyte draw)



DIABETES INSIPIDUS

Disease where kidneys and ADH do not work together properly

CENTRAL DI

ADH not being made/secreted


Treatment: ADH

NEPHROGENIC DI

Kidneys not responding to ADH production


Treatment: drink lots of water!

OSMOLAR GAP NORMAL

10-15

INCREASED OSMOLAR GAP

Alcohols/low molecular weight substances

ANION GAP

#Cations-#Anions


(difference between charges in body)

DECREASED ANION GAP

Myeloma


(if negative; this is a machine error!)

INCREASED ANION GAP

From acidosis


(increased Sodium; increased positive charges)

SODIUM

MOST ABUNDANT EXTRACELLULAR CATION


135-145


(Impacts the plasma volume)

HYPONATREMIA

Sodium <130 by renal or non-renal losses

HYPONATREMIA OVER-CORRECTION

Added salt will attract water...even water from brain....pull it off = death

PESUDOHYPONATREMIA

Sodium not actually low; use direst ISE

HYPERNATREMIA

Sodium >150 by renal or non renal gains

POTASSIUM

MAJOR INTRACELLULAR CATION


3.5-5.5


(30x more inside cells than out)

HYPOKALEMIA

Potassium <3.0


Associated with Alkalosis

HYPERKALEMIA

Potassium >6.0


Associated with Acidosis

RENAL HYPERKALEMIA

GFR<20; decreased kidney function

CELLULAR HYPERKALEMIA

Caused by:


Leukemia/muscle injury: shift in cell production

GI HYPERKALEMIA

Caused by:


Increased potassium intake coupled with poor renal function

PSEUDOHPYERKALEMIA

Caused by:


-Hemolysis: (cell lysis letting K+ out)


-Thrombocytosis: (platelets filled with K+)


-Turniquet: (prolonged use)

TUMOR LYSIS SYNDROME

Potassium is leaking out of the cells that are being killed and causing increased serum levels

RENAL TUBULAR ACIDOSIS

Cannot reabsorb enough bicarbonate

BICARBONATE

Second highest EXTRACELLULAR ANION

CHLORIDE

MAJOR EXTRACELLULAR ANION


98-108


(maintains electrical neutrality)

MAGNESIUM

Coupled anion with calcium for muscles


-regulated by kidney and PTH

VITAL HORMONES

Cortisol, Insulin and T4

FOLLICLES

Line the outside of Thyroid; need iodine

TSH

Thyroid Stimulating Hormone; produce T3/T4

TOTAL THYROXINE

Total T4: measure of what has been picked up by TBG and what is free in blood

FREE THYROXINE

Measure of T4 that is not bound to proteins

DEIONIDASE

Enzyme that converts T4 to T3

THYROGLOBULIN

Stores thyroid hormones

T3

The active form of thyroid hormone;


Present in 1000x less than T4

HASHIMOTOS THYROIDITIS

Hypothyroidism: measured TPO & Tg Antibody


Destroys the thyroid gland


Decreased T4/T3


Increased TSH from feedback to pituitary


Dry skin, dry hair, slow speech


Give patients T4



GRAVES DISEASE

Hyperthyroidism: antibody mimics TSH


Increased T3/T4


Decreased TSH by feedback


Weightloss, heat intolerance


Give Patients I131

HPA AXIS

Hypothalamus, pituitary, Adrenal (ACTH), cortisol

CORTISOL

Steroid hormone: needed for stress response, increasing blood glucose levels, immune system suppression....

PRIMARY ADDISONS DISEASE

Hypoadrenalism: issue with adrenal itself


Decreased Cortisol


Increased ACTH (by feedback)


Increased MSH, Decreased Aldo


Treat: cortisol replacement therapy


(ACTH test)

SECONDARY ADDISONS DISEASE

Hypoadrenalism: issue with pituitary


After cortisol treatment pituitary "goes to sleep"


Caused by: coming off of cortisol too quickly


Decreased ACTH (shrunken adrenal)


(ACTH test)

ADDISONIAN CRISIS

Insufficient adrenal steroid production for the point in time


Decreased Blood pressure


Decreased Blood Sugar

PANHYPOPITUITARISM

HPA Axis is "off"


Decreased ACTH, Cotrisol...etc

ACUTE ADRENAL HYPOFUNCTION

Caused by Meningitis


Several hemorrhage impacts adrenal

CUSHINGS DISEASE

Hyperaldrenalism: pituitary tumor


Increased ACTH, increased Cortisol


Increased Blood Sugar, decreased T Cells


"moonface, buffalo hump..."


(urinary free cortisol test)

CUSHINGS SYNDROME

Hyperadrenalism: caused by doctor


Giving too much cortisol!



HYPERCORTISOLISM

Caused by: Adrenal Tumor


Increased Cortisol with Decreased ACTH


Treat: remove the tumor!

HYPERALDOSTERONISM

Will keep the sodium and remove potassium


Increased Aldo and Sodium


Decreased Renin and Potassium


Treat: remove tumor!


(spot urine test to see K+)

CONGENITAL ADRENAL HYPOPLASIA

21-OH Deficiency: salt losing type


Defect in enzyme making aldosterone


Backup steroid precursor (andestenedione DHEA)


Ambiguous genitailia & "infant hercules" boys

MEDULLA

Produces "fight or flight" hormones


CATECHOLAMINES

Modified amines produced by Medulla


Give instant stress response


(dopa, dopamine, norepinephrine, epinephrine)

PHEOCHROMOCYTOMA

Adult medulla tumor


Secretes Epinephrine & norepinephrine


Mimics anxiety: panic attacks, weightloss...


(VMA and Metonephrines) in 24 hour urine



NEUROBLASTOMA

Baby and Kid Medulla Tumor


Secretes Dopamine


Increased HR, BP, diarrhea, spine malignancy


(HVA test)

OSMOTIC FORCE

Why molecules want to pull water along w them



HYPOTONIC SOLUTION

Draws salt out of cells so they burst


Lyses them

HYPERTONIC SOLUTION

Draws water out of cells so they shrivel

NEPHRON

Combined glomerulus and tubules


1,000,000 per kidney


halves in the body by age 80

NEPHROSIS

State w/ leaky glomerular basement membrane


Caused by thickening or change in charge


Proteinuria, edema, hypoalbuminuria, waxy cast

POST STREPTOCOCCAL GLOMERULONEPHRITIS

Antigen/Antibody complex stuck in kidneys


Activates complement


RBC casts, bleeding, "lumpy bumpy"

GOOD PASTURES SYNDROME

Nephritis caused by Ab directed to GBM


Antigen builds up on membrane


Causes linear "ribbon candy" fluorescence

BUN

Blood Urea Nitrogen


Should be 8-25


Only increases after 60-70% of nephrons ruined

CREATININE:

Should be 0.6-1.3


Filtered only in small amounts


Increases only with very low GFR

CREATINE

Normal muscle energy storage


Increases proportionately to muscle mass

UREA

Main end product of nitrogen metabolism

UREMIA

Accumulation of nitrogenous wastes


Protein -> Amino Acids -> Urea



AZOTEMIA

Nitrogenous waste buildup that is toxic


Due to increased protein catbolism or impaired kidney function

PRE-RENAL AZOTEMIA

Not enough blood getting to the kidney


-low urine sodium

RENAL AZOTEMIA

Kidney itself if sick


-high urine sodium

POST-RENAL AZOTEMIA

Outflow is obstructed (prostate, stone, tumor)


-increased kidney pressure, BP, dead tubules

ANURIA

Cessation of urine flow


Caused by: BOTH kidneys failing


OR the only urethra being blocked

SPECIFIC GRAVITY

Test indicates tubule ability to concentrat/dilute


Should be 1.010-1.030

PLASMA SPECIFIC GRAVITY

1.010

MAXIMUM SPECIFIC GRAVITY

1.030

VASODILATION

Influences kidney perfusion

NSAIDS

Inhibit vasodilation


Vasoconstruction squeezes blood vessels


Deadly in elderly with poor kidney function

RAAS

Renin, Angiotension, Aldosterone System

RENIN

Enzyme that makes angiotensinogen


Converts to Angiotensin I in lung


Converts to Angiotensin II for Aldosterone

SCARRED VESSELS

Decreased perfusion, increased relative solute absorption, decreased osmolarity, increased renin, increased alsodteron, increased sodium

HYPOTHALAMUS

Has osmoreceptors to monitor [salt/solute]


Changes ADH levels

ADH

Antidiuretic Hormone

HYPERTONIC DCT REACTION

Too much sodium, sends ADH to stop peeing and retain water to return to isotonic

HYPOTONIC DCT REACTION

Too much water, stops ADH to increase peeing

ESRD

End stage Renal Disease: requires dialysis


GFR<15

HEMODIALYSIS

3x weekly occurance


Requires vascular access


Complications with Staph Epi

EXTRA KIDNEY HORMONES

1, 24-OH Vitamin D and Erythropoietin


Renal failure requires Epo injections

PTH

Relied on to regulate calcium levels from kidney

PYELONEPHRITIS

Kidney infection


With WBC, Bacteria and WBC casts

CYSTITIS

Bladder infections


With WBC, bacteria but NO WBC casts

ACUTE TUBULAR NECROSIS

Hypo perfusion causing PCT cells to die


-Dirty brown (granular casts)


-Increased urinary sodium (cant reabsorb)

DRUG INDUCED ATN

Caused by antibiotics, NSAIDS, diuretics


-Eosinophilia; use Hansel Stain


-IgE

GLOMERULOSCLEROSIS

Thickened basement membrane of capillary loops; seen in diabetics


-scarring & most common cause of ESRD


-microalbuminura


>30mg/g of creatinine

FECUNDABILITY

Maximum fertility in life; around age 25


Falls off after 30

HIGH RISK PREGNANCY

Beyond age 35


Increased Chromosomal & non abnormalities


Autosomal recessive

INFERTILITY

Inability to conceive after 12 months unprotected sex

FSH

Follicle stimulating hormone;


develops the follide

LH

Leutinizing Hormone


Triggers ovulation based on estrogen levels

OVULATION

Actual release of the egg

BASAL BODY TEMPERATURE

Changes throughout menstrual cycle


Lowest on last day of follicular (1st) phase

ESTROGEN

Steroid hormone from ovarian follicle


Changes throughout the cycle

E1

Estrone: weak hormone


Associated with menopause

E2

Estradiol:


Associated with reproductive years


FIRST HALF OF CYCLE



E3

Estriol:


Associated with pregnancy

PROGESTERONE

Steroid made from cholesterol


SECOND HALF OF CYCLE


-Low without ovulation

POST-MENOPAUSE

Decreased estradiol


Decreased progesterone


Increased LH/FSH by feedback

AROMATASE

Converts testosterone into estrogen in women



AROMATASE INHIBITORS

Used to block receptors in breast cancers

HcG

Human Chorionic Growth Hormone


Double every 2-3 days during first 12 weeks

ORAL CONTRACEPTIVES

Inhibits ovulation, alters cervical mucus, alters endometrium, lowers estrogen