5 normal processes important to endocrine function
biological rhythm, blood pressure, fluid volume, metabolism & nutrient availability, and mineral control & electrolyte balance
mammary gland hormone
prolactin
thyroid gland hormone
TSH
adrenal gland hormone
ACTH (stress hormone)
gonads hormone
FSH/LH
hormone linked to growth of target cells
somatostatin
hormone linked to melanocytes
MSF (linked to cancer)
hormone in direct control of BP
adrenal epinephrine
hormone with indirect control of BP
norepinephrine
adrenal epinephrine stimulated by
sympathetic nervous system
4 actions of epinephrine and norepinephrine on BP
MAP increased, increased Ca++ to heart cells, vasoconstriction of arteries in abdominal circulation w/ vasodilation of muscle, and relaxed bronchial smooth muscle to increase ventilated zones
long term control of fluid volume by
hypothalamus
hormones related to fluid volume
vasopressin and renin-angiotensin aldosterone system
hormone that causes water retention and is triggered by increase in CSF osmolarity
vasopressin
purpose of this system is to increase fluid osmolarity so water moves from cells to vessels and potassium is lost in the urine (affected by sodium)
renin-angiotensin-aldosterone system
6 hormones involved in control of metabolism & nutrient availability
hormone associated with calcium control, released when there is a high blood Ca++ to cause increased bone absorption of calcium
calcitonin
hormone associated with calcium control, when there is low blood Ca++ to cause absorption of calcium from bone
parathyroid hormone
4 groupings of endocrine disorders
hyperendocrine, hypoendocrine, primary, and secondary
excessively high blood concentrations of a hormone
hyperendocrine
endocrine disorder caused by secreting tumors or excessive stimulation of the gland by trophic signals
hyperendocrine
excessively low blood concentrations of a hormone
hypoendocrine
endocrine disorder caused by failure or congenital absence of glandular tissue, surgical removal of the gland, or lack of normal trophic signals
hypoendocrine
direct malfunction of hormone producing gland
primary endocrine disorder
malfunction of hypothalamus/pituitary cells that control hormone producing gland
secondary endocrine disorder
endocrine disorder caused by intrinsic defects within the hormone secreting gland
primary endocrine disorder
endocrine disorder caused by abnormal pituitary secretion of trophic signals
secondary endocrine disorder
dysglycemia with impaired glucose tolerance (an intermediate between normal and diabetes) and impaired fasting
pre-diabetes
constellation of cardiometabolic risk factors including dyslipidemia, obesity, glucose intolerance, and hypertension; group of disorders with insulin resistance as a main feature
metabolic syndrome
disorder of glucose tolerance not diagnostic of diabetes characterized by fasting blood glucose value between 100 and 126
impaired fasting glucose
disorder of glucose tolerance not diagnostic of diabetes characterized by 2 hour post-prandial blood glucose value between 140 and 200
impaired glucose tolerance
an endocrine disorder characterized by impaired glucose entry into insulin sensitive cells due to an absolute or relative deficiency of insulin
diabetes mellitus
8 signs of insulin resistance
acanthosis nigricans, skin tags, hirsutism, acne, menstrual irregularities, android appearance in women, virilization, male pattern vertex balding
Characterized by an absolute insulin deficiency caused by pancreatic cell failure; two forms include immune-mediated and idiopathic DM
type 1 diabetes mellitus
Beta-cells of the pancreas are destroyed, resulting in loss of insulin production. Immune mediated: Associated with certain HLA genetic makeup; may be autoimmune; viral infection or exposure to a toxic agent may be a responsible environmental influence.
immune-mediated T1DM
Associated with beta-cell destruction without autoimmune markers.
idiopathic T1DM
Characterized by a relative insulin deficiency caused by decreased tissue sensitivity and responsiveness to insulin; risk factors include aging, sedentary lifestyle, obesity, and genetic predisposition.
type 2 diabetes mellitus
caused by delayed meals or snacks, increased exercise or activity, alcohol intake without food, intensive insulin therapy, medication errors
treatment includes ingestion of glucose or carbohydrate containing food
hypoglycemia
diabetic emergency most common in T1DM
diabetic ketoacidosis
diabetic emergency most common in T2DM
NKHHC
caused by hyperglycemia, sudden onset precipitated by infection, stress, inadequate insulin dose
diabetic ketoacidosis
symtpoms include hot and dry skin, dehydration, Kussmaul respirations, fruity or ETOH or acetone breath, blood glucose >250, positive ketones, polyuria, polydipsia, and polyphagia
diabetic ketoacidosis
treatment includes supplemental insulin, fluid and electrolyte replacement, and medical monitoring
diabetic ketoacidosis
caused by hyperglycemia, onset is gradual precipitated by infection, stress, or poor fluid intake
NKHHC
symptoms include profound diaphoresis and dehydration
NKHHC
treatment includes insulin and rapid IV fluid replacement
NKHHC
rebound hyperglycemia following an episode of hypoglycemia caused by counter regulatory hormone release (check blood glucose at 2am)
somogyi effect
A marked increase in insulin requirements between 6 am and 9 am as compared with the midnight to 6 am period.
6 alterations in physiologic function associated with microvascular complications of diabetes
blindness, ESRD/CKD, foot ulcers, sexual dysfunction, infections, gastroparesis
aka gallstones, Chief complaint of most patients is biliary colic, a persistent epigastriac or right upper abdominal pain. A typical episode lasts several hours. Brought on by a meal or may occur at night.
cholelithiasis
refers to inflammation of the gallbladder wall. It is classified as acute or chronic, according to its clinical manifestations
cholecystitis
Characterized by severe right upper abdominal pain that may radiate to the back. Present in about 90% of patients. Bacterial infection may be present although it is not thought to be the direct cause.
acute cholecystitis
an important subgroup of acute cholecystitis. Tends to occur in the setting of major surgery, critical illness, trauma, or burn related in jury. Pts tend to be male and older than 50.
acalculous cholecystitis
inflammation of the gallbladder wall due to persistent low grade irritation from gallstones. Diabetes and obesity are important predisposing factors
chronic cholecystitis
most common causes are are hemolysis and ineffective erythropoises. The reabsorption of hematomas in patients with mild liver disease is a common cause of mild jaundice due to unconjugated hyperbilirubinemia.
prehepatic jaundice
dysfunction of each of the hepatic steps in bilirubin metabolism may cause this type of jaundice
hepatic jaundice
RNA virus that is spread by the fecal-oral route. There is a 2-7 week incubation period. May be asymptomatic or mildly symptomatic without jaundice. This is diagnosed through serologic testing. Presence of IgG indicates previous infection
hepatitis A
partially double stranded DNA virus, has an incubation period of 2-6 mos. Infection is longer and more insidious than HAV and may involve a variety of immune complex related phenomena, including urticaria, arthritis, serum sickness, and glomerulonephritis
hepatitis B
Single stranded RNA virus that belongs to the Flavivirus family. Worldwide about three percent of the population is chronically infected. Mode of transmission of closely resembles HBV, although sexual and perinatal transmission are much less likely.
hepatitis C
may coincide with or succeed HBV infection and requires its presence for replication. This disease is primarily transmitted by parenteral routes and by intimate personal contact
hepatitis D
may be the most common cause of acute hepatitis in the developing countries. Cases in developed countries are usually related to recent travel. An RNA virus spread via the fecal-oral route, especially through contaminated water
hepatitis E
a group of diseases characterized by inflammation of the liver that lasts six months or longer. The condition may be idiopathic, autoimmune, or metabolic. It may also follow acute viral hepatitis or may be caused by hepatotoxic drugs or toxins.
chronic hepatitis
often called triaditis. Chronic, low grade liver inflammation of any cause. Condition may be asymptomatic or may be associated with mild, nospecific symptoms. Progressive liver disease does not usally develop, and no drug treatment is indicated.
chronic persistent hepatitis
a PROGRESSIVE destructive inflammatory disease that extends beyond the portal triad to the hepatic lobule. Symptoms typical of acute hepatitis are often seen. Eventually chronic active hepatitis often culminates in cirrhosis and end stage liver disease
chronic active hepatitis
generally classified as hepatitis A, B, C, D, and E
acute viral hepatitis
also known as enteric, because it is generally transmitted by ingestion of contaminated substances. Flu-like symptoms are less severe than HBV symptoms. Early treatment with y-globulin and vaccination after exposure may be effective in preventing disease.
hepatitis A
known as Serum Hepatitis because its usually route of transmission is through infected blood. Incubation period is longer and the severity of symptoms (jaundice) greater than in HAV
hepatitis B
known as non A and non B. Resembles HBV in route of transmission. Develops in 85% of cases and is usually asymptomatic until advanced liver disease intervenes. Treatment is with intramuscular pegylated interferon and oral ribavirin for 6 -12 months.
hepatitis C
coinfects with HBV and requires the presence of HBV to be active
hepatitis C
Prevention of HBV infection also prevents
hepatitis D
common virus in the developing world that causes an illness similar to HAV but has a HIGH MORTALITY RATE in pregnant women
hepatitis E
characterized by persistent inflammation of the liver lasting six mornths or more. Automimmune disease, viral hepatitis, (B and C), toxins and metabolic disease may cause this, and it may progress to cirrhosis.
chronic active hepatitis
6 major structures of the GI tract
Mouth, pharynx, esophagus, stomach, and small and large intestines
5 accessory GI structures
salivary glands, the pancreas, and the biliary system. (liver, gallbladder, and bile ducts)
4 general functions of the GI tract in providing nutrients for the body
motility, secretion of digestive juices, digestion of nutrients, and absorption of nutrients.
mostly in the form of triglcyerides but also include phospholipids, cholesterol, and fat soluble vitamins A, D, E, and K. Digestion occurs in the small intestine, where fats are emulsified by bile.
lipids
composed of amino acids, undergoes digestion in the small intestine includes sources from food and from enzymes, digestion begins in the stomach.
proteins
digestion is initiated by the mouth by salivary amylase. Pancreatic amylase continues this process in the small intestine.
complex carbs
black blood found in drainage or excreta, such as feces
melena
feces containing bright red blood
hematochezia
blood in vomitus
hematemesis
Inflammation of the stomach and intestines, which may occur on an acute or chronic basis and is commonly caused by viruses
gastroenteritis
A progressive and irreversible loss of renal function over months to years defined by glomerular filtration rate of <60ml/min for 3 months or more
Renal fx remains normal ________% of nephrons are damaged
75-80%
stage of CRF characterized by Decreased renal reserve: <75% nephron loss. Clinical findings: no S&S, BUN and creatinine normal, may not be diagnosed
stage 1 CRF
stage of CRF characterized by renal insufficiency: 75-90% nephron loss. Clinical findings: polyuria, nocturia, slight elevation in BUN and creatinine, may be controlled by diet and meds
stage 2 CRF
stage of CRF characterized by 90% nephron loss. Clincial findings: azotemia, uremia, fluid and electrolyte abnormalities, renal osteodystrophy, dialysis or transplant necessary. Fluid volume overload develops, aka ESRD
stage 3 CRF
3 reasons for obstructive urinary disease
anatomic abnormalities such as ureteral valves, strictures of the urethral meatus, and stenosis at the ureterovesical or ureteral pelvic junction
factors that predispose an individual to renal calculi
maintaining fluid and electrolyte homeostasis and ridding the body of water soluble wastes
amount of fluid filtered per hour by renal system
7L
renal system alters amount and composition of urine in order to
maintain normal blood volume and electrolyte composition within the body
2 endocrine functions of renal system
production of erythropoietin and vit. D
what determines the filtrate volume
net filtration pressure
what determines the filtrate concentration as being permeable or non-permeable
capillary permeability
permeable components in renal function
H2O, electrolytes, glucose, urea, creatinine, or drugs
non-permeable components in renal function
bld cells, platelets, plasma protein
2 variables that can be adjusted to change the filtration rate
glomerular hydrostatic pressure and plasma osmolarity
reabsorbs 2/3 of the filtered water, electrolytes, HCO3, glucose, amino acids, and vitamins
proximal convoluted tube
actively reabsorbs Na, K, Cl to produce a hypoosmotic filtrate and a high interstitial osmolality
ascending loop of Henle
reabsorbs Na (due to Aldosterone), H2O (due to vasopressin), Cl, urea, and HCO3 (due to pH). It also secretes H and K, ammonia and PO4
distal convoluted tube
reabsorbs water under the influence of ADH and secretes H and K
collecting tubule
endocrine control that increases water permeability and reabsorption in the last portion of the distal tubule and collecting tubule
ADH
endocrine control that stimulates bone marrow to produce and secrete RBC in response to tissue hypoxia
erythropoietin
endocrine control that converts Ca to the active form and reabsorption occurs in the intestine
vitamin D
endocrine control that inhibits Na absorption in the collecting ducts and increases urine formation
atrial natriureatic factor
used to determine the renal disease by the presence of urinary casts
urinalysis
used to determine how much of a substance can be cleared from the body by the kidneys per a given amount of time
serum creatinine clearance
freely filtered substance, as well as insulin, and neither are reabsorbed or secreted so you can compare both to any substance (X) to determine the renal handling of (X)
creatinine
If creatinine clearance = clearance rate (X) then
X is neither secreted nor absorbed
If creatinine clearance > clearance rate (X) then
X is reabsorbed
If creatinine clearance < clearance rate (X) then
X is secreted
Reflects glomerular filtration and urine concentrating capacity and is the end product of protein breakdown
blood urea nitrogen
BUN increases as GFR ________
decreases
BUN is a better measurement of
ARF
5 factors that affect BUN
dehydration, altered protein intake, protein catabolism, ARF, and CRF
a collection of symptoms caused by the glomerular disease. It is characterized by an increase of glomerular capillary wall permeability to serum proteins. The predominant abnormality is the loss of large amts of protein in the urine (>3.5g/d)
nephritic syndrome
causes a disturbance in the glomerular basement membrane
diabetic nephropathy
manifestations of nephritic syndrome
hypoprotienemia, hypoalbuminemia, edema, hyperlipidemia, and hypercoaguability
inflammation of the glomerulus caused by immunologic abnormalities, ischemia, drugs, and toxins. Most common cause of ESRD. The epithelial layer of the glomerulus membrane is disturbed with loss of negative charges and change in membrane permeability
glomerulonephritis
2 pathos of glomerulonephritis
1) Deposition of circulating antigen-antibody complexes and formation of antibodies specific to glomerular membrane and 2) Activation of biochemical mediators of inflammation, altered membrane permeability and other alterations
2 manifestations of glomerulonephritis
Hematuria (smokey brown-tinged urine and RBC casts) and Protienuria (exceeding 3-5g/d and primarily albumin)
a sudden, severe decrease in renal fxn that is potentially reversible. Associated with a decrease in GFR, oliguria (<500ml/d), and azotemia.
acute renal failure
Abrupt reduction in renal fxn with an elevation of BUN and creatinine levels
acute renal failure
decrease bld flow to kidneys leading to ischemia and necrosis
pre-renal failure
etiology of Pre-RF
Shock, CHF, pulmonary embolism, anaphylaxis, sepsis, and pericardial tamponade
obstruction of the urinary collecting system anywhere from the calyces to the urethral meatus
post-renal failure
etiology of Post-RF
urethral/bladder cancer, renal calculi, prostatic hyperplasia or cancer, cervical cancer, or urethral stricture
acute tissue damage to the kidney
intra-renal failure
etiology of intra-RF
nephritis, toxins, glomerulonephritis, vasculitis, ATN, renal artery or vein stenosis
phase of ARF that begins within 1day of hypotensive events, lasts 1-3weeks (varies with duration of ischemia or severity of injury), urine output may vary 10-20% is nonoliguric (<500mg/d), BUN and creatinine concentrations increase.
oliguric phase
phase of ARF with prompt onset with urine flow increasing rapidly, urine output up to 10L/d, electrolyte losses, BUN starts to fall, usually lasts 2-3weeks, and tubular fxn resumes
diuretic phase
phase of ARF where client begins to return to normal activity but the kidney fxn may not return to normal
recovery phase
– progressive loss over months to years. GFR <60ml/min. Advancement can sometimes be slowed, but it is ultimately irreversible and terminates into end-stage renal disease (ESRD)
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