Path 2 Exam 1 Study Guide

Chemical Messengers

initiate pre-programmed responses in target cells; some act distally or locally

Trophic hormones

signal release of other hormones

Paracrine Hormones

local action on cells other than the releasing cells

Autocrine Hormones

Local action on releasing cells themselves

What are the primary actions of hormones

Released by gland/cell, circulated in bloodstream, reach target cell, specific action

Target cells response varies according to what factors

Number of receptors and affinity of receptors

Humoral control

capillary blood contains low concentrations of Ca2+ which stimulates the parathyroid glands and thyroid gland to secrete PTH

Neural control

preganglionic SNS fiber stimulates adrenal medulla cells to secrete catecholamines

Hormonal control

hypothalamus secretes hormones that stimulate the anterior pituitary gland to secrete hormones that stimulate other endocrine glands to secrete hormones

Hypothalamus

receives input from multiple sources and communicates with the pituitary gland to stimulate releasing and inhibiting factors

Pituitary Gland

'master gland',

* releases many hormones that either affect target cells or signal the release of other hormones

Growth Hormone

'GH or Somatotropin' from pituitary gland, promotes bone and muscle growth, protein synthesis, fatty acid mobilization, and growth of visceral, endocrine organs, and connective tissues

ADH

* antidiuretic hormone

released from the pituitary gland, causes the kidneys to decrease urine output and increase the body's water content

TSH

* thyroid-stimulating hormone

trophic hormone released by the pituitary gland affecting the thyroid gland

ACTH

* adrenocorticotropic hormone

trophic hormone released by the pituitary gland affecting the adrenal cortex

Calcitonin

Released by the thyroid gland to reduce blood calcium leves that inhibits osteoclasts

T3 and T4

released by thyroid gland to increase metabolic rate, protein synthesis, and normal growth and development of nervous system in children

PTH

* Parathormone

released by the parathyroid gland to regulate (increase) blood calcium and phosphorus levels

Thymosin

released by thymus gland to stimulate maturation of T-lymphocytes

Mineralocorticoids

released by adrenal cortex, specifically aldosterone to influence sodium and water absorption and potassium excretion

Glucocorticoids

released by adrenal cortex, specifically cortisol to raise blood glucose levels, affect metabolism of all nutrients, and have an anti-inflammatory response

Sex hormones (androgens)

released by adrenal cortex to help convert testosterone and dihydrotesterone peripherally

Epinephrine and norepinephrine

neurotransmitters released by adrenal medulla for the sympathetic nervous system

Primary endocrine disorders

Defects originates in the gland

Secondary endocrine disorders

defect in level of stimulating hormone or releasing factor

Tertiary endocrine disorders

dysfunction of hypothalamus, both the pituitary and target organ are understimulated

ADH hypersecretion

the body retains too much water causing hypervolemia, called SIADH

ADH hyposecretion

the body releases too much water through urine causing dehydration

GH deficiency

In children-dwarfism, characterized by short stature

GH excess

\n In children, gigantism characterized by tall stature, In adults, acromegaly characterized by larger bones of hands, feet, and face

Hyperthyroidism

increased metabolic rate in almost all body tissues with characterizations of increased ventilation, heart rate, blood volume, vasodilation, appetite, intestinal motility, weight loss, fine tremors, restlessness, nervousness, anxiety, difficulty sleeping, sweating. Can be caused by hyperactive thyroid gland (grave's disease), goiter, or pituitary or thyroid tumor

Hypothyroidism

generalized decrease in metabolic rate with manifestations of decreased ventilation, heart rate, blood volume, appetite, intestinal motility, weight gain, sluggish mental and physical function, somnolence

Hyperparathyroidism

increased blood calcium levels resulting in abnormal nerve conductions and muscle contractions as well as demineralization of bone

Hypoparathyroidism

decreased blood calcium levels resulting in abnormal nerve conductions and muscle contractions

Adrenal cortex hyperfunction

much more common than hypo, cushing syndrome manifests with 'buffalo hump and moon face', facial hair, thinning scalp

Adrenal cortex hypofunction

addison's disease, relatively rare, manifests with hypoglycemia, hypotension, dehydration, hyperpigmentation of skin, sparse body hair in women

Thyroid cortex Hypofunction

\n rare but life-threatening complication of hyperthyroidism characterized by very high fevers and extreme cardiovascular and central nervous system effects

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Role of liver in maintaining blood glucose levels

glycogenesis, glycogenolysis, gluconeogenesis

Describe the endocrine function of the pancreas

creates insulin from beta cells and glucagon from alpha cells

Insulin Function

\n only hormone that directly lowers blood glucose, also facilitates in glucose uptake by target cells, glycogenesis, inhibits breakdown of fat and glycogen, increases protein synthesis

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Glucagon function

increases blood glucose via negative feedback, helps with maintenance between meals and when fasting, and released during strenuous activity

relationship between the pancreas and the liver in blood sugar control

Pancreas releases glucagon when blood sugar levels are too low, glucagon stimulates the liver to breakdown glycogen, glycogen is then turned to glucose in the liver, thus raising the blood sugar levels. In contrast, when the blood sugar levels are too high, the pancreas releases insulin, which stimulates glucose uptake from the blood and stimulates formation of glucose into glycogen in the liver, thus lowering blood sugar.

Type 1 DM

caused by a destruction of beta cells in the pancreas which results in absolute insulin deficiency, most commonly an autoimmune issue. These patients will require exogenous insulin to prevent hyperglycemia, catabolic state, and ketosis. The onset for these patients are sudden, usually

Type 2 DM

caused by a relative insulin deficiency from several metabolic abnormalities such as peripheral insulin resistance, initial hyperinsulinemia progressing to beta cell failure, or increased glucose production by the liver. The typical onset of these patients is adult ages, however many children in the US has this, the onset is slower and the body build is typically obese.

What is Gestational DM?

A glucose intolerance occurring during pregnancy. This can result in higher risks of complications, mortality, fetal abnormalities, and may or may not lead to diabetes mellitus after pregnancy.

Urine Testing (DM)

Seen infrequently to be used

Blood Testing (DM)

fasting blood glucose (FBG), casual blood glucose, oral glucose intolerance test (OGTT), glycated hemoglobin (A1C)

Fasting blood glucose (DM)

at least 8 hours after last meal, normal

Casual blood glucose (DM)

no regard to last meal, >200 mg/dL diabetes

Oral glucose tolerance test (DM)

assesses blood glucose 1 hour and 2 hours after ingestion of 75 grams of concentrated glucose, normal when blood glucose returns to normal in 2-3 hours (

A1C (DM)

\n current gold standard, normally glucose is not incorporated into hemoglobin, mean plasma glucose correlated with hemoglobin A1C, recommended A1C levels

What is Metabolic syndrome?

when people have type 2 MB, they usually have a syndrome of metabolic abnormalities such as hyperglycemia, obesity, hyperlipidemia, hypertension, systemic inflammation, vascular disease

What are the cardinal signs of DM?

3 polys', polyuria, polydipsia, polyphagia

Polyuria

Excessive Urination

Polydipsia

Excessive thirst

Polyphagia

excessive eating from excessive appetite or hunger

hyperglycemia

blurred vision, fatigue, paresthesia, skin infections

Diabetic ketoacidosis

rate of ketone production exceeds cellular use and renal excretion resulting in metabolic acidosis

Hyperglycemic hyperosmolar state

excessively high blood glucose (>600 mg/dL) that can result in cellular dehydration and many CNS manifestations, most common in type 2 DM

Discuss the chronic complications associated with DM

microvascular diseases such as neuropathy, nephropathy, retinopathy, macrovascular complications, foot ulcers, orthopedic problems, infections, impaired healing

Peripheral neuropathy

ischemia of nutrient vessels and segmental demyelination, a direct effect of hyperglycemia

Nephropathy

progressive lesions affecting kidney function, eventual end-stage renal disease

Retinopathy

\n within 20 years of diagnosis, nearly all type 1 and 60% type 2 have some degree of cataracts, glaucoma, or retinal detachment

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Discuss the treatment/management options for DM

diet, exercise, and medications

hypoglycemia

\n sweating, trembling, dizziness, mood changes, hunger, headaches, blurred vision, extreme tiredness and paleness

Discuss the signs and symptoms of hyperglycemia

dry mouth, fruity breath, extreme thirst, frequent urge to urinate, drowsiness, frequent bed wetting, stomach pain

Liver lobule

hexagonal plates of hepatocytes, contains kupffer cells that are phagocytic and antigen presenting cells

Hepatic Triad

location of hepatic portal vein, hepatic artery, and bile duct at each corner of lobule

Discuss the Hepatic Portal System

the venous system that returns blood from the digestive tract and spleen to the liver

What is the function of Kupffer cells?

phagocytic, antigen presenting cells

Bilirubin

pigment derived from hemoglobin, the liver converts this into conjugated bilirubin which gives feces its normal color

function of the gallbladder

Bile stored and some bile modifications

Describe the various ducts associated with bile transportation

right and left hepatic duct -> common hepatic duct -> cystic duct -> common bile duct -> duodenum

Metabolic regulation (liver)

all via the hepatic portal system, all blood leaving digestion must pass through the liver. The liver then stabilizes blood glucose levels through gluconeogenesis and glycogenolysis. The liver also regulates circulating lipid levels and helps with amino acid metabolism. The liver also helps with waste product removal and converts ammonia to urea. It also plays a part in removal and breakdown of all circulating drugs as well as storage for vitamins and minerals.

Hematologic regulation (liver)

phagocytosis of activated T cells, ingested and self-antigens, breakdown of old RBCs, plasma protein synthesis, removal of hormones, toxins, and antibodies

Bile synthesis (liver)

comprised of water, ions, bilirubin, cholesterol, and bile salts

What is bile?

liquid involved in emulsification and enhances activity of lipases

Discuss the exocrine function of the pancreas

creates pancreatic juice that contains digestive enzymes, water, and ions

signs and symptoms of hepatic pathology?

right upper quarter pain, skin changes, urine and stool changes, neurologic changes, blood and fluid disorders, possible other GI symptoms

Portal HTN

elevated blood pressure, results in backflow of pressure through portal system resulting in ascites, splenomegaly, hemorrhoids, and esophageal varices

Jaundice

yellow skin color and sclera of eyes, due to hyperbilirubinemia, often first and only symptoms of liver disease; this can be caused by excessive bilirubin production, failure of hepatocytes to remove, conjugate, and excrete bilirubin, or insufficient excretion of bile

Asterixis

flapping tremors or liver flap, inability to maintain wrist extension with shoulders flexed

Fatty Liver Disease

\n fatty deposits in hepatocytes, either alcoholic or non-alcoholic

Hepatitis

\n inflammation of the liver, various groups (A, B, C, D, E), various modes of transmission, incubation periods, mechanisms, and degree of liver damage, capacity to evolve to carrier state, diagnosed through blood work

HAV

oral-fecal route, generally benign, self-limiting, vaccine available

HBV

can be transmitted through most body secretions, longer incubation and greater severity than HAV, greater risk for acute hepatitis, chronic hepatitis, cirrhosis, vaccine available

HCV

transmitted via blood or blood products, most people chronically infected but asymptomatic, greatest risk for chronic liver disease, no vaccine at present

Cirrhosis

progressive inflammation and scarring of the liver tissue and ducts, the end resulting in liver failure

Hepatic Encephalopathy

\n altered mentation, LOC, other neurologic signs due to buildup of ammonia, urea

Liver CA

primary or secondary (more common and metastatic), usually hepatocellular carcinoma or cholangiocarcinoma, usually not diagnosed until advanced and poor 5-year survival rate

Liver failure

can be from sudden, massive events or chronic, progressive conditions; results in liver transplant needed

Cholelithiasis

gall stones, results from water in bile reabsorbed in gall bladder making it supersaturated, can be a/symptomatic and has the potential for period attacks

Cholecystitis

caused by impaction of gall stones, distention and ischemia of gall bladder

signs and symptoms of gall bladder pathology?

pain in upper right quarter, heart burn, may steadily worsen, coincides with eating, anorexia, indigestion, nausea, vomiting, diarrhea

Pancreatitis

\n inflammation of the pancreas, can be caused by microorganisms, blockage of ducts, ischemia, reaction to toxin

What is metabolism

Sum total of all chemical reactions

How is adipose tissue related to nutrition?

90% of energy stored here, contains adipocytes that uptake, synthesize, store, and mobilize lipids

Leptin

decrease food intake, increase energy expenditure

Ghrelin

Regulates food intake, body weight and glucose homeostasis

Carbohydrates

4 kcal/g, transformed into glucose for energy or stored in the liver, three types- simple, complex, or fiber