Unit 3 Flashcards
Proton pump inhibitors
-prazole
Gastric ulcers
Histamine H2 receptor blockers
-idine
Gastric ulcers
Oral antidiabetics
-amide
Antidiabetic type 2
Bisphosphonates
-dronate
Osteoporosis
Hypothalamus
center of the endocrine system, negative feedback, controls pituitary
Adipose tissue
endocrine gland, secretes hormones for metabolism. Adinoectin and leptin. White vs Brown fat
Phychoimmunology
endocrine, NS, and immune system interact.
Sympathetic NS
is aroused during stress and causes the adrenal medulla to release catecholamines
Catecholamines
compounds that control stress response, fight or flight. Epinephrine, norepinephrine, dopamine
Cortisol
Glucocorticoid hormone from adrenal cortex, lipid and carb metabolism, stress response
Decrease: Wound healing, inflammation, bone formation
Increase: urine, GI secretions
Endorphins
Endogenous, modulate pain transmission
Growth Hormone (Somatotrophin)
Stimulates skeletal and visceral growth, increases after stress
Prolactin
Growth of breasts and milk, sexual satisfaction
Testosterone
regulate male sex characteristics
Neuroendocrine Theory of Aging
Cells are programed to die or lose function (menopause)
Aging Pituitary
Decrease in weight and blood supply
Aging Thyroid
Decrease in size, becomes fibrotic, decreases hormone secretion
Aging parathyroid
no changes
Aging Adrenal Glands
Increase fibrotic
Carpal Tunnel Syndrome
Common with acromegaly, diabetes, pregnancy, hypothyroidism
Posterior Pituitary
Only stores and releases hormones; Oxytocin and ADH
Oxytocin
Stimulates contractions, breast milk, and sleep rhythm
ADH
Vasopressin; reabsorbtion of water at kidneys and ACTH Release
Anterior Pituitary
Makes and stores hormones; Somatotropin, TSH, FSH, LH, Prolactin, ACTH, Lipotropin, MSH
Thyroid Stimulating Hormone
TSH; secretes Thyroxine (T3) and Triiodothyronine (T4)
Follicle Stimulating Hormone
Sex organs, develop follicle, estrogen secretion, and sperm maturation
Luteinizing Hormone
Ovulation, corpus luteum maintenance, progesterone and testosterone secretion
Adrenocorticotrophic Hormone
Adrenal cortex, release of corticosteroids
Lipotrophin
Break down fat and synthesize and corticosteroids
Melanocyte Stimulating Hormone
Produced melanin
Hyperpituitarism
Acromegaly, Carpal tunnel, over growth of body
Acromegaly
Excessive secretion of GH, affects face, hands, and head
Thyroid Gland
Produces Thyroxine (T3) and Triiodothyronine (T4) and calcitonin
Calcitonin
When calcium is high, calcitonin increases calcium excretion to lower blood levels
Parathyroid Hormone
When calcium is low, PTH increases calcium reabsorption and bone demineralization to lower blood levels; Stimulated by TSH
Hyperthyroidism
Increase in metabolic function; women more than men 4:1, Graves disease is common 85%, thyroid storm
Graves Disease
- Thyroid-stimulating immunoglobulins that react against thyroglobin; stimulates enlargement and excess secretion
-Increases SNS
-Hyperthyroidism, increased T4 production
Hyperthyroidism Clinical Manifestations
-Goiter: enlarged thyroid
-Increased: Nervousness, heat intolerance, tremors, heart palpitations
-Exophthalmos: protruding eyes
-Peri-Arthritis: tendon inflammation
-Myopathy: muscle weakness, dyspnea
Hyperthyroidism Diagnosing
Increased TSH, antithyroid hormones, TSI
Hyperthyroidism Therapy
Antithyroid medication, surgery, Radioiodine
Hyperthyroidism PT Implication
Exercise intolerance and capacity
Hypothyroidism
Generalized slowed metabolism; congenital or removal
Hypothyroidism Type I
Low functioning thyroid or impaired release; altered lipid metabolism
Hypothyroidism Type II
failure of the pituitary to release TSH
Hypothyroidism Clinical Manifestations
Neuromuscular: decreased function and stiffness
Myxedema: non pitting edema of hands, feet, and scapula
Rheumatic symptoms
Hypothyroidism Diagnosing
Increased: TSH, cholesterol, phosphate, triglycerides
Decreased: T4
Parathyroid
Secrete PTH, on thyroid, 2
Hyperparathyroidism
Overactive parathyroid; disrupts calcium, phosphate and bone metabolism
Primary Hyperparathyroidism
Glands enlarge and interrupt PTH secretion
Secondary Hyperparathyroidism
-hypocalcemia
-glands become hyperplastic
Tertiary Hyperparathyroidism
Dialysis with long term secondary Hyperparathyroidism, glands become unresponsive
Hyperparathyroidism Clinical manifestations
Hypercalciuria, bone damage (osteoporosis), kidney damage, decreased NS function, muscle atrophy, GI disruptions
Hypoparathyroidism
Hypocalcemia; increased phosphate, NS irritability; decreased Ca+
Iatrogenic: Acquired, most common, gland damage or removal
Idiopathic: children, genetic or autoimmune
Hypoparathyroidism Clinical Manifestations
Neuromuscular irritability and calcification of organs
Adrenal Glands
Glands on kidneys, responses to stress
Adrenal Cortex
Secretes mineralocorticoids, glucocorticoids and androgrens
Mineralocorticoids
steroid hormones for fluid imbalances; aldosterone
Glucocorticoids
steroid hormones for metabolism of glucose, suppresses inflammation and immune functions; cortisol
Androgens
sex hormones, affect gonads
Adrenal Medulla
Secretes epinephrine and norepinephrine
Epinephrine
Fight or flight, increases response (adrenaline)
Norepinephrine
Same as epinephrine
Primary Adrenal Insufficiency
Addison Disease; insufficient cortisol release; removal/injury/radiation/cancer/infection
1) Decreased Cortisol Production
2) Aldosterone Deficiency
Primary Adrenal Insufficiency Pathogenesis: Decreased Cortisol production
less glucose production, Ca+, and stress resistance, weakness, increased ACTH
Primary Adrenal Insufficiency Pathogenesis: Aldosterone Deficiency
Fluid imbalances, increased NA excretion, dehydration, decreased heart activity
Primary Adrenal Insufficiency Treatment
Increase cortisol and fluids
Primary Adrenal Insufficiency PT Implications
Limited Stress (Addisonian crisis)
Secondary Adrenal Insufficiency
ACTH suppression = cortisol deficiency only
1) steroids
2) infection
3) pituitary removal
Adrenocortical Hyperfunction
Hypercorticolism, excess cortisol
Cushing Syndrome, Cushing disease, and Pseudo-Cushing syndrome
Cushing Syndrome
Hypercortisolism;
1) Hyperfunction of adrenal
2) Excess corticosteroids
3) excess ACTH
Cushing Disease
over secretion of ACTH from pituitary
Pseudo-Cushing Syndrome
emotional response causes symptoms
Adrenocortical Hyperfunction Clinical Manifestations
Hyperglycemia, high BP, muscles weakness, osteoporosis
Adrenocortical Hyperfunction Diagnosis
increased cortisol in urine and blood
Adverse Effects of Glucocorticoids
Mood, skin, GI, Bone, Fluid retention, infection, weakness
Conn Syndrome
Primary aldosteronism; adrenal glands hypersecrete aldosterone due to tumor; increases NA+ reabsorption
Adipokines
Proteins released by fat cells; autocrine hormones; decrease appetite
Visceral Fat
Bad, around abdomen releases cytokines that cause CVD and inflammation
bariatrics
study of obesity and weight management
Underweight BMI
<18.5
Normal BMI
18.5-24.9
Overweight BMI
25-29.9
Obese BMI
> 30
Obese Class I BMI
30-34.9
Obese Class II BMI
35-39.9
Obese Class III BMI
> 40
Type 1 DM
5-10%, abrupt, autoimmune
Type II Dm
90-95%, insulin resistance from B cell stress
Normal Glucose Lab values
A1C: 5.7%
Fasting: 99
GTT: 140
Prediabetes Glucose Lab Values
A1C: 5.7-6.4%
Fasting: 100-125
GTT: 140-199
Diabetes Glucose Lab Values
A1C: 6.5<%
Fasting: 126<
GTT: 200<
Prevalence of Diabetes
1/10
Prevalance of Prediabetes
1/3
Incidence of people that don’t know: Diabetes
1/5
Incidence of people that don’t know: Prediabetes
8/10
Pathogenesis of DM
- Decreased utilization of glucose
- Increased fat mobilization
- Decreased Protein utilization
Diabetes Clinical Manifestation
polydipsia, weight loss, fatigue, neuropathy, vision issues, infects, polyphagia, non-healing wounds, polyuria
Macrovascular Complications of DM
-Arteries to heart, lungs, brain
-Heart disease
-stroke
-atherosclerosis
Microvascular Complications of DM
-eye issues,
-peripheral nerves
-kidney failure
-infections
Hypoglycemia
-Low glucose, rapid onset, shaking/dizziness/headache, tachycardia, tremors, insulin shock
Hyperglycemia
-high glucose (>250), gradual, fruity breath, high ketones, polyuria
Diabetic Ketoacidosis
common in Type 1, Triad:
-Hyperglycemia
-acidosis
-ketosis
Goal for DM remission
A1C: <7%
BP: <130/80
Low LDL, high HDL
Endogenous opioid peptides
Released to control pain and inflammation, regulates immune, GI and Cv
Endorphins, enkephalins, dysorphins
Opioid receptors
Mu: sedation, respiratory depression, constipation
Kappa: sedation
Delta: growth hormone
Strong Agonists Opioids
-severe pain
-Mu receptors
-Morphine, tramadol
Mild to Moderate Opioids
-moderate pain
-Codeine, oxycodone
Mixed Agonist-Antagonists Opioids
-agonist and antagonist activity
-Activate kappa while partially blocking Mu
Antagonist Opioids
-no pain relief
-treats overdoses and addiction
Opioid Uses
-Preop
-general anesthesia
-cough suppressant
-severe diarrhea
-NOT for sharp, intermittent pain
Opioid Mechanism of action
-Decreased Afferent pain transmission and neuron excitability
-Increased efferent activity that decreases pain
Opioid Spinal Effects
Receptors bind to pre/post-synaptic membranes of spine
Opioid Supraspinal Effects
-Bind to grey matter of midbrain and decrease pain from descending pathways
-Increase activity of descending pathways that release serotonin, norepinephrine, and inibits pain
Opioid Peripheral Effects
Decreased excitability and transmission of primary sensory nerve endings
Opioid Adverse effects
Mental slowing (narcotic), Respiratory depression, hypotension, GI distress
Opioid Induced Hyperalgesia
-increased pain sensitivity or lack of response to meds
-worsens at the peak of drugs
-hypothesized due to increase glutamate
Methadone
milder withdrawl symptoms
Buprenorphine
mixed agonist-antagonist
Glucocorticoids
-cortisol
-carbohydrate and protein metabolism
Mineralocorticoids
-aldosterone
-regulate electrolytes and water metabolism
Corticosteroids
-used for immunosuppression and adrenal insufficiency
-Hormones produced by adrenal cortex
-Increase blood glucose
-Decrease WBC, inflammatory response, vascular permeability
Adverse effects of corticosteroids
Increased:
Glucose metabolism, hyperglycemia, weight gain
Decreased:
Puberty
Adverse effects of Glucocorticoids
-Mood/sleep
-Skin
-GI irritation
-Bone loss
-FLuid retention
-Infection
-Muscle weakness
NSAIDs
Decrease inflammation, pain, body temp, blood clotting
Archidonic Acid Derivatives
Leukotriene (LOX): inflammation, asthma
Cycolooygenase (COX): fever reducer, NSAIDS inhibit on
-Prostaglandins
-Thromboxane
COX-1
Gastric protection, platelet function
COX-2
Pain, fever, bone formation, inflammation, cell response to stress, cell division
-Selective NSAIDs inhibit this
Asprin Function
-COX 1&2 inhibitor
-Decrease pain, inflammation, fever, blood clotting, heart conditions, stroke, cancers
Adverse effects of Asprin
-GI problems
-Cardiovascular issues (increase BP)
-Kidney function
-Overdose
-Reyes
-Inhibit healing (bone and wound)
COX-2 Selective drugs
-Decrease GI distress and clotting
-Increase CV events
Ways to combat GI distress from NSAIDS
-Histamine blockers
-Proton Pump
-Drugs that mimic prostaglandins
Acetaminophen
-Not NSAIDs
-Non inflammatory
-Liver issues with too much
Enteric NS
-Brain of bowel
-Functions independently of CNS
-Emotions, brain, and GI system
Achalasia
-Swallowing disorder
-Failure to relax muscles
GI Distress Symptom from Exercise
Cramping, fecal urgency, diarrhea, burping, nausea/vomiting, heartburn
Neurogenic Causes of Diarrhea
Hyperthyroidism
Neurogenic Causes of Constipation
IBS, CNS lesions, dementia
Muscular Causes of Diarrhea
Electrolyte imbalance, endocrine disorder
Muscular Causes of Constipation
Pelvic floor muscles, obstruction
Mechanical Causes of Diarrhea
Incomplete obstruction, post op, diverticulitis
Mechanical Causes of Constipation
Obstruction, tumor, pregnancy
Other Causes of Constipation
Diet, opioids, dehydration
Other Causes of Diarrhea
Diet, antibiotics, laxative, malabsorption, IBS
Hiatal Hernia
-Esophageal hiatus becomes enlarged, stomach passes through diaphragm
-Sliding hernia (90-95%)
-Rolling Hernia (5-10%)
Hiatal Hernia Risk Factors
Things that weaken diaphragm and increase intrabdominal pressure
Hiatal Hernia Clinical Manifestations
-heartburn
-Reflux
Hiatal Hernia PT Implications
-Avoid laying flat
-Avoid valsalva
-avoid abdominal pressure
Gastroesophageal Reflux Disease (GERD)
-reflux of gastric contents from lower esophageal spincter
-erosive or non-erosive
-10-20% of adults
GERD Causes
-low pressure of LES, foods, smoking, bad drinks, positioning, pregnancy
GERD Clinical Manifestations
Heartburn
Extra-esophageal:
-Asthma, cough, laryngitis
GERD Treatment
-lifestyle modifications
-Antacids, h2 blockers, proton pump inhibitors
Peptic Ulcer Disease (PUD)
-break in lining of stomach or duodenum
-Gastric, duodenal, stress
PUD Causes
Mucosal layer balance, foods, apsrin, H. Pylori
PUD Clinical Manifestations
Bleeding, perforation, penetration (erodes to other organs)
Inflammatory Bowel Disease
-polygenic disease with complex interactions with gut microbiota
-Crohn, ulcerative colitis
Extra-intestinal manifestations
-arthritis
Crohn’s Disease
-chronic inflammatory disease that can affect the intestinal tract
-has lesions
-less body growth
Ulcerative colitis
-chronic inflammatory disorder of mucosa of colon
-usually rectum and left colon
-bloody stools
-cancer common
Inflammatory Bowel Disease PT Implications
-low back pain, psoas abscess, joint issues, osteoporosis
Diverticulosis
-outpouchings in the wall of the colon or SI
-herniate through muscular layers of colon
Diverticulitis
inflammation/infection of diverticula
Diverticular Disease Clinical Manifestations
Uncomplicated:
-mild symptoms of pain
Complicated:
-fistula may develop with bladder, pneumaturia, fecaluria, UTIs
Appendicitis
-inflammation of the vermiform appendix that results in necrosis
-15-19 years
Appendicitis Causes
-obstruction of lumen
-Bacterial infections
Appendicitis Clinical Manifestation
-Abdominal pain, anorexia, nausea/vomiting, low-grade fever
-pain is constant and may shift within 12 hours
-McBurneys point
-WBC >20,000
Rectum Fissure
-ulceration or tear of lining of anal canal
-excessive tearing
-sharp pain, burning, spasms
Hemorrhoids
Varicose veins inder mucosal membranes in lower anus and rectum
Internal hemorrhoids
lower rectum, bleeding in stool
External hemorrhoids
-under skin around anus, bleeding, nerve-rich tissue
-medications
Liver Function
-digestive, endocrine, excretory, hematologic, and immune
-conversion of bilirubin
-clotting factors
-metabolize drugs
-filters blood
-albumin
Pancreas
Exocrine Gland
-digestive juices, neutralize acids
Endocrine Gland
-secretion of glucagon and insulin
Gallbladder
-bile reservoir
-release bile
Liver Disease Symptoms
-hepatic osteodystrophy
-dark urine
-light feces
-RUQ pain
-GI symptoms
-Edema
Hepatic Failure
-liver cells sufficiently diminished due to cirrhosis, liver cancer, inflammation
Clinical Syndrome
-Hepatic encephalopathy: neuromuscular dysfunction due to decreased liver function
-Renal failure
-jaundice
Jaundice
-yellow discoloration of the skin (>2)
-yellow/ dark urine and stool (>3)
- Overproduction of bilirubin
- Decreased bilirubin metabolism
- Hepatocyte dysfunction
- Impaired bile flow
Spider Angiomas
vascular manifestations of increased estrogen levels or liver disease
Palmar erythema
warm redness of the skin over palms from liver failure
Neurologic Symptoms
-confusion, sleep disturbances, muscle tremors, hyper-reactive relaxes
-impaired PNS function
-hepatic encephalopathy
Asterixis
-flapping tremors or Liver Flap
-inability to maintain wrist extension with forward flexion of UE
-tremor absent at rest
MSK Symptoms liver disease
-thoracic pain b/wn scapula, right shoulder, trapezius
Hepatic Osteodystrophy
-abnormal development of bone
-most common symptom
-osteomalacia or osteoporosis
-pain in wrist
Aging Hepatic System
-liver decreases in size, weight and blood flow
-increase time to process
-less tolerant to damage
-decreased albumin production
-decreased immune functions
Liver Drug Distribution w/ Age
-albumin decreases, drugs that bind might need increased dosages
-increased fat mass increases lipophilic drug distribution
Liver Disease Complications
-Jaundice
-cirrhosis
-portal hypertension
-hepatic encephalopathy
-ascites
Cirrhosis
-irreversible inflammation of the liver
-liver damage
-loss of normal tissue
Portal Hypertension
-elevated portal pressure entering liver is higher than IVC
-fibrosis contributes
-Blood backs up into other areas
Hepatic Encephalopathy
-neuropsychiatric syndromes from subtle to motor disturbances
-Gi bleeding, infection, hypovolemia
Ascites
-accumulation fo fluid in peritoneal cavity
-caused by liver cirrhosis, heart failure
-dyspnea
- pericentesis and diacritics
Spontaneous bacterial Perotonitis:
-infection of ascitic fluid with portal hypertension
Hepatitis
-inflammation of the liver caused by a virus
-ABCDEF
Chronic hepatitis
-several diseases for >6 months
-most asymptomatic
Acute Liver Failure
-rare, but can be fatal
-develops over days to weeks
-Most caused by acetaminophen hepatotoxicity
Viral hepatitis
-ABCDEF
-long incubation period
-easily spread
-symptoms:malaise, fatigue, fever, nausea/vomiting, anorexia
Hepatitis A
-fecal to oral
-contaminated water or food
-transmission highest during incubation (15-50 days)
-acute only
Hepatitis B
-highly infectious
-STD
-Percutaneously transmitted (skin puncture and blood)
-2-5 months incubation
-can stay in blood for 1 wk
Hepatitis C
-injection use
-can become chronic
-2 wks- 6m
Hepatitis D
-uncommon in US
-superinfection of Hep B
Hepatitis E
-uncommon in US
-contaminated water
-fecal to oral
Hepatitis F
-Fulminant Hepatitis
-acetaminophen hepatoxicity
-severe, sudden, sometimes fatal
Alcoholic Liver Disease
-Alcoholic steatosis (fatty liver): <3 bilirubin, elevated AST & ALT enzymes
-Alcoholic steatohepatitis: only histologic diagnosis
-Alcoholic hepatitis: >3 bilirubin, elevated AST & ALT enzymes, fibrosis
-Cirrhosis
Alcoholic Liver Disease Pathogenesis
-fatty liver disease
-alcohol stresses hepatocytes
-liver responds to inflammation by scarring
Alcoholic Liver Disease Treatment
-nutrition
-liver transplant
-corticosterioids
-stop alcohol
Nonalcoholic Fatty Liver Disease
-fatty liver disease without inflammation
-asymptommatic
Nonalcoholic Hepatic Steatosis
Nonalcoholic Steatohepatitis
Acute Pancreatitis
-inflammation of pancreas
-2/3 involve gallstones and alcohol
-Mild or moderately severe
-interstitial or necrotizing
-back pain, GI symptoms, weight loss
Mild Acute Pancreatitis
-absence of organ failure
Moderately Severe Pancreatitis
-organ failure, RUQ pain, back pain
Interstitial Acute Pancreatitis
-80% of cases
-mild
Necrotizing Acute Pancreatitis
-20% of cases
-higher mortality
Severe Acute Pancreatitis
-cytokines and free radicals create systemic response
-fever, tachycardia, hypoxia, tachypnea
Fluid changes
Chronic Pancreatitis
-irreversible changes to pancreas of chronic inflammation
-activation of stellate cells leading to fibrosis
-abdominal pain, back pain, worse with meals, 90% of function loss
Pancreatic Cancer
-3rd leading cause of cancer morality
-lowest 5 year survival rate
-95% adenocarcinoma (75% head of pancreas)
-History of T2D
Pancreatic Cancer Clinical Manifestations
-vague
-abdominal pain
-weight loss
-jaundice
-obstruction of portal vein
-diabetes
Pancreatic Cancer Metastasis
-Lymph nodes to liver to lungs to bone to adrenals
-tumors at body and tail are 2x more likely to metastasize
Chole-
bile
Cholang-
bile ducts
Cholangiography
Radiographic study of bile ducts
Cholangitis
-inflammation of bile duct
-obstruction and stasis of bile from stones
-Charcot Triad: pain, fever, jaundice
-Reynolds Penad: charcot triad plus hypotension
Cholecyst-
gallbladder
Cholecystectomy
removal of gallbladder
Cholecytitis
-inflammation fo gallbladder
-prolonged abdominal pain
cholecystography
radiographic study of gallbladder
cholecystostomy
incision and drainage of gallbladder
Choledocho-
common bile duct
choledocholithiasis
stones in common bile duct
choledochostomy
exploration of common bile ducts
Cholelith-
gallstones
Cholelithiasis
-presence of gallstones
-gallstone disease
-75% cholesterol
-25% bilirubin
-Most common symptoms in cystic duct
-abdominal pain
Cholescintigraphy
radionuclide imaging of biliary systems
Cholestasis
stoppage or suppression of bile flow
