SIADH pathology
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-Overproduction of ADH
-Increased permeability of renal tubules to water and increased water
reabsorption
-Enhanced water retention and increased total body water...water
intoxication
-Excess water retention results in hyponatremia (dilutes sodium levels)
-Urine sodium excretion = sodium intake
-Serum hypo osmolarity & urine hyperosmolarity
abdominal hernia
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, can get strangulated in muscle wall—possible obstruction; possible
ischemia
diabetic neuropathy
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-Sensory deficits (loss of pain, temperature, vibration)
-painful peripheral neuropathy
-wrist/foot drop
-autonomic neuropathy-
-altered bladder control,
-orthostatic hypotension
secondary hypothyroidism
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affects the negative feedback loop- pituitary. T3/T4 low, TSH low
sx of duodenal ulcers
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Hypersecretion of stomach acid and pepsin
Sx: chronic intermittent pain in epigastric area
Pain begins 2-3 hours after eating
Pain is RELIEVED w/ food intake; Pain-food-relief pattern
Constant, unremitting pain often caused by complications
, Complications: bleeding, perforation, obstruction of stomach or duodenum
outlet d/t edema, scaring
type 1 DM
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absolute insulin deficiency; Chronic (lifelong) disease that results from
absolute lack of insulin from loss of beta cells
-Results from autoimmune destruction of beta cells and is believed to be
result of genetic and environment interaction
-Diagnosis is rare before 9 months of life and peaks at 12 years of age
-Historically has abrupt onset
-Currently presents with long preclinical stage with immune destruction of
beta cells leading to insulin deficiency and hyperglycemia
-Most common type is type 1A (80-90% of cases) with beta cell auto
antibodies and antibodies against insulin
-Triggered by environmental factors such as drugs/chemicals, certain
foods, or viruses
Slowly progressive autoimmune T cell mediated disease that destroys
bbeta cells
-occurs as a secondary pathology that results from such diseases as
pancreatitis which destroys the beta cells resulting in hyperglycemia
cirrhosis
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, PATHO:
-Irreversible inflammatory disease, disrupts liver function and structure
-Decreased hepatic function caused by nodular and fibrotic tissue
synthesis (fibrosis)
-Biliary channels become obstructed, cause portal hypertension
· S/S Jaundice; Edema; Hemorrhoids; etc PPT slide 71
· CAUSES: Alcoholism
prodromal phase: hepatitis sx
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2 weeks after exposure; fatigue, anorexia, malaise, N & V, RUQ pain. Ends
with appearance of jaundice. HIGHLY TRANSMISSIBLE IN THIS PHASE!!
s/sx of Addison's Disease
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Mild to moderate cases: weakness and easy fatigue.-Hyperpigmentation
(Darkening of the skin - patchy skin color and vitiligo (areas of no pigment)
may occur
-As condition progresses: anorexia, nausea and vomiting and diarrhea;
weight loss
**Biggest concern: development of hypotension and vascular collapse and
shock
why do we see visual problems with pituitary tumors?
Give this one a try later!
Give this one a try later!
-Overproduction of ADH
-Increased permeability of renal tubules to water and increased water
reabsorption
-Enhanced water retention and increased total body water...water
intoxication
-Excess water retention results in hyponatremia (dilutes sodium levels)
-Urine sodium excretion = sodium intake
-Serum hypo osmolarity & urine hyperosmolarity
abdominal hernia
Give this one a try later!
, can get strangulated in muscle wall—possible obstruction; possible
ischemia
diabetic neuropathy
Give this one a try later!
-Sensory deficits (loss of pain, temperature, vibration)
-painful peripheral neuropathy
-wrist/foot drop
-autonomic neuropathy-
-altered bladder control,
-orthostatic hypotension
secondary hypothyroidism
Give this one a try later!
affects the negative feedback loop- pituitary. T3/T4 low, TSH low
sx of duodenal ulcers
Give this one a try later!
Hypersecretion of stomach acid and pepsin
Sx: chronic intermittent pain in epigastric area
Pain begins 2-3 hours after eating
Pain is RELIEVED w/ food intake; Pain-food-relief pattern
Constant, unremitting pain often caused by complications
, Complications: bleeding, perforation, obstruction of stomach or duodenum
outlet d/t edema, scaring
type 1 DM
Give this one a try later!
absolute insulin deficiency; Chronic (lifelong) disease that results from
absolute lack of insulin from loss of beta cells
-Results from autoimmune destruction of beta cells and is believed to be
result of genetic and environment interaction
-Diagnosis is rare before 9 months of life and peaks at 12 years of age
-Historically has abrupt onset
-Currently presents with long preclinical stage with immune destruction of
beta cells leading to insulin deficiency and hyperglycemia
-Most common type is type 1A (80-90% of cases) with beta cell auto
antibodies and antibodies against insulin
-Triggered by environmental factors such as drugs/chemicals, certain
foods, or viruses
Slowly progressive autoimmune T cell mediated disease that destroys
bbeta cells
-occurs as a secondary pathology that results from such diseases as
pancreatitis which destroys the beta cells resulting in hyperglycemia
cirrhosis
Give this one a try later!
, PATHO:
-Irreversible inflammatory disease, disrupts liver function and structure
-Decreased hepatic function caused by nodular and fibrotic tissue
synthesis (fibrosis)
-Biliary channels become obstructed, cause portal hypertension
· S/S Jaundice; Edema; Hemorrhoids; etc PPT slide 71
· CAUSES: Alcoholism
prodromal phase: hepatitis sx
Give this one a try later!
2 weeks after exposure; fatigue, anorexia, malaise, N & V, RUQ pain. Ends
with appearance of jaundice. HIGHLY TRANSMISSIBLE IN THIS PHASE!!
s/sx of Addison's Disease
Give this one a try later!
Mild to moderate cases: weakness and easy fatigue.-Hyperpigmentation
(Darkening of the skin - patchy skin color and vitiligo (areas of no pigment)
may occur
-As condition progresses: anorexia, nausea and vomiting and diarrhea;
weight loss
**Biggest concern: development of hypotension and vascular collapse and
shock
why do we see visual problems with pituitary tumors?
Give this one a try later!
