Adult 1 Exam 4 Review

obesity

BMI above 30

\-prevalence higher in women, African American, and Hispanic

causes of obesity

\-behavioral

\-environmental

\-physiologic

\-genetic

obesity associations

\-6-20 year decrease in life expectancy

\-risk for cancer increases with increased BMI

\-likelihood of type 2 diabetes by tenfold

\-asthma/hypertension by fourfold

\-twice as likely to have alzhemiers

overweight

BMI 25-29.9

obese

BMI exceeding 30

Severe/extreme obese

BMI exceeding 40

diabetes diagnosis

\-symptoms of diabetes + random blood glucose of 200 mg/dL

\
\-fasting plasma glucose of 126 mg/dL

\
\-hemoglobin A1C>6.5%

\
\-2-H plasma glucose of 200 mg/dL during an oral glucose tolerance test

diabetes risk factors

\-family history

\-obesity (BMI>= 25 kg/m^2)

\-physical inactivity

\-African American, Latino, Native American, Asian American, Pacific Islander

\-History of Gestational Diabetes

\-Hypertension

type 1 diabetes

beta cell destruction

type 2 diabetes

insulin resistance and/or secretory defect

functions of insulin

transports and metabolizes glucose for energy

\-inhibits glycogenolysis and gluconeogenesis

\
\-stimulates storage of glucose in the liver and muscle as glycogen

\-signals liver to stop the release of glucose

\-enhances storage of dietary fat in adipose tissue

\-accelerates transport of amino acids into cells (K+, too)

glycogenolysis

liver turning glycogen into glucose

gluconeogenesis

lactate and amino acids into glucose

type 1 diabetes

\-Insulin-producing beta cells in the pancreas are destroyed by an influx of lymphocytes (resulting cytokines TNF-a, Interferon-g, Interleukin 1)

\
\-Decreased function of pancrease to produce functional insulin to regulate glucose metabolism

\
\-When glucose cannot be metabolized it will get converted and stored as fat (liver) Genetic – predisposition – human leukocyte antigen Immunologic – autoimmune – signs can be detected years before symptom onset environmental factors

\
\
results in: decreased insulin production, unchecked glucose production by the liver and fasting hyperglycemia

insulin absence

body does not metabolize carbohydrates

body signals

liver to convert fat to glucose for energy

ketone metabolism

produces increase in acid production creating an acidotic state

bhb

a ketone that is measurable and as the anion gap closes the levels of BHB decrease

type 2 diabetes

insulin resistance and impaired insulin secretion

\-affects 95% of adult with diabetes

\-onset over age 30 years

\-increasing in children

\-slow, progressive glucose intolerance and may go undetected for years

latent autoimmune diabetes of adults

\-Subtype of diabetes in which progression of autoimmune beta cell destruction in the pancreas is slower than in types 1 and 2 diabetes

\-not insulin dependent in the initial 6 months of disease onset

\-clinical manifestation of LADA shares the features of types 1 and 2 diabetes

\-emerging subtype has led some to propose the diabetes classification scheme should be revised to reflect changes in the beta cells in the pancreas

type 1 risk factors

\-early onset

\-familial

\-genetic predisposition

\-possible immunologic or environmental (viral or toxins) facotrs

type 2 risk factors

\-obesity

\-age

\-previous identified impaired fasting glucose/impaired glucose tolerance

\-hypertension >= 140/90 mm Hg

\-HDL

medical management of diabetes

\-main goal is to normalize insulin activity and blood glucose levels to reduce the development of complications

\
\-the ADA now recommends HgbA1c less than 7%

diabetes management components

\-nutritional therapy

\-exercise

\-monitoring

\-pharmacologic therapy

\-education

meal planning

\-carbohydrates: 50-60% carbohydrates; emphasize whole grains

\-fat: 30%, limiting saturated fats to 10% and

glycemic index

\-combining starchy foods with protein and fat slow absorption and glycemic response

\
\-raw or whole foods tend to have lower responses than cooked, chopped, or pureed foods

\
\-eat while fruits rather than juices; this decrease glycemic response because of fiber

\-adding foods with sugars may produce lower response if eaten with foods that are more slowly absorbed

hypoglycemia

abnormally low blood glucose level (below 50-60); too much insulin/oral hypoglycemia agents, excessive physical activity and not enough food

\-adrenergic symptoms: sweating, tremors, tachycardia,palpitations, nervousness, hunger

\-CNS Symptoms: inability to concentrate, headache, confusion, memory lapses, slurred speech, drowsiness

\
severe hypoglycemia: disorientation, seizures, loss of consciousness, death

hypoglycemia management

\-give 15g/fast acting concentrated carbohydrate (3/4 glucose tablets, 4-6 oz of juice/regular soda)

\
\-retest blood glucose in 15 minutes; retreat is >70 or if symptoms persist more than 10-15 minutes and testing is not possible

\
\-provide a snack with protein and carbohydrates unless pt plans to eat a meal within 30-60 minutes

diabetic ketoacidosis

\-absence/inadeqaute amount of insulin resulting in abnormal metabolism of carbohydrate, protein and fat

\
clinical features: hyperglycemia, dehydration, acidosis

dka assessment

blood glucose levels >300-1,000

\
\-is reflected in low serum bicarbonate, low pH, low PCO2 reflects respiratory compensation (kussmaul respirations)

\-ketone bodies in blood and urine

\-electrolytes vary according to degree of dehydration; increase in creatinine, Hct, BUN

DKA treatment

\-rehydration with IV fluid- glycemic diuresis

\-IV continuous infusion of regular insulin

\-reverse acidosis and restore electrolyte balance

oral antidiabetic agents

\-used for pts with type 2 diabetes who require more than diet and exercise along

\-combinations of oral drugs may be used

\-major side effect: hypoglycemia

\-nursing interventions: monitor blood glucose for hypoglycemia and other potential side effects

hyperglycemia hyperosmolar syndrome

\-caused by a lack of sufficient insulin;ketosis is minimal or absent

\-hyperglycemia causes osmotic diuresis, loss of water and electrolytes, hypernatremia, and increase osmolality

hhs manifestations

\-hypotension

\-profound dehydration

\-tachycardia

\-variable neurologic signs caused by cerebral dehydration

\-high mortality rate-particularly if corrected too quickly

hhs treatment

\-rehydration

\-insulin administration

\-monitor fluid volume and electrolyte status

\
prevention;

\-BGSM

\-Diagnosis and management of diabetes

\-Assess and promote self-care management skills

chlorproprmide

(Diabenase)-first generation sulfonyureas

\
\-stimulate pancrease

\-increase insulin recepteors

second generation sulfonylureas

\-glipizide, glyburide

\
\-stimulate beta cells-increase insulin production

\-caution with beta-blockers

alpha glucosidase inhibitors

acarbose (Precose)

\
\-decrease absorption of carbohydrates (do not increase insulin)

\-take with food

\-contraindication: GI, Kidney or Liver (cirrhosis) Dysfunction

\-monitor liver function

biguanide

metformin (glucophage)

\-inhibits glucose production by the liver

\-may impact renal function

\-do not give if pt is receiving contrast media

\
\-caution: lactic acidosis

dpp 4 inhibitors

sitagliptin (Januvia), vildagliptin (Galvus)

\
\-increase insulin levels by increasing action of incretin

\-once daily

\-monitor renal function

glp 1 agonists

dulaglutide (Trulicity)

\
\-enhances glucose dependent insulin secretion

\-once daily

\-may impact renal function

sglt 2 inhibitors

empaglilozin (Jardiance)

\
\-icnrease glucose excretion by the kidney

\-Type 2 only

thiazolidinediones

pioglitazone (Actos), rosiglitazone (Avandia)

\
\-increase tissue sensitivity/responsiveness to insulin

\-monitor liver function

\-oral contraceptives: increased risk of pregnancy

bile

empties into the duodenum and reabsorbed in the distal ileum (enterohepatic circulation)

metabolic function of liver

\-glucose metabolism-glycogenolysis, gluconeogenesis

\
\-ammonia conversion-amino acids for gluconeogenesis, converts ammonia to urea for excretion

\
\-protein metabolism-protein synthesis, vitamin K, clotting factors

\-fat metabolism-fatty acids→ketones→energy→fatty acids→ cholesterol, etc.

\
\-vitamin and iron storage

\-bile formation-bile salts from cholesterol→ emulsification of fats

\
\-bilirubin excretion-byproduct of Hgb breakdown→ small intestine and urine and bile

\-drug metabolism-first pass metabolism

first pass metabolism

drugs absorbed in the gut are biotransformed (metabolized) in the liver

liver function studies

\-serum aminotransferase: AST, ALT, GGT, GGTP, LDH

\-serum protein studies

\-direct and indirect serum bilirubin, urine bilirubin and urobilinogen

serum aminotransferases

indicators of injury to the liver cells;useful in detecting hepatitis

alanine aminotransferase

levels increase primarily in liver disorders;used to monitor the course of hepatitis, cirrhosis, the effects of treatments that may be toxic to the liver

aspartate aminotransferase

not specific to liver disease however levels of AST may be increase in cirrhosis, hepatitis, and liver cancer

gamma-glutamyl transferase

levels are associated with cholestasis;alcoholic liver disease

jaundice

bilirubin levels exceed 2 mg/dL

\
yellow discoloration due to increase serum bilirubin in sclera, skin and urine

4 types of jaundice

hemolytic

hepatocellular

obstructive

hereditary hyperbilirubinemia

portal hypertension

obstructed blood flow through the liver results in increased pressure throughout the portal venous system

\
results in: ascites and esophageal varices

ascites causes

\-portal hypertension resulting in increased capillary pressure and obstruction of venous blood flow

\
\-vasodilation of splanchnic circulation (blood flow to the major abdominal organs)

\
\-changes in the ability to metabolize aldosterone, increasing fluid retention

\
\-decrease synthesis of albumin, decreasing serum osmotic pressure

\
\-movement of albumin into the peritoneal cavity

esophogeal varices

occurs in about 1/3 of patients with cirrhosis and varices

\
\-1st episode: mortality rate 10-30% depending on severity

\-high risk for re-bleeding: \~70%

\
\-second episode: 30-50%

esophogeal varices manifestations

hematemesis, melena, general deterioration and shock

varices treatment

\-treat for shock;administer oxygen

\-IV fluids, electrolytes, volume expanders, blood and blood products

\-vasopressin

\-somatostatin

\-octreotide

\-nitroglycerin

\-propanolol and nadolol

\-balloon tamponade

vasopressin

decreases mesenteric blood flow/vasoconstriction

somatostatin

decrease GI motility and splanchnic blood flow

octreotide

constricts arterioles in the splanchnic bed, decrease portal hypertension

nitroglycerin

in combination with vasopressin, reduces coronary vasoconstriction with varices

propanolol and nadolol

decrease portal pressure-used in combination with other treatment

pancrease exocrine

amylase, trypsin, lipase, secretin

pancrease endocrine

insulin, glucagon, somatostatin

choleliathisis

when a patient has calculi in the gallbladder

medical management of cholelithiasis

\-ERCP

\-Dietary management

\-medications: ursodeoxycholic acid and chenodeoxycholic acid

\
\-laparascopic cholecystectomy

\
\-nonsurgical removal

cholelithiasis post op interventions

\-low fowler position

\-NG/NPO until bowel sounds return; then a soft, low fat, high-carbohydrate diet

\-care of biliary drainage system

\-analgesics, pain management

\-turn, cough, and deep breathing;splinting to reduce pain

\-abulation

\-self care education

acute pancreatitis

pancreatic duct becomes obstructed and enzymes back up, causing auto-digestion and inflammation of the pancreas

chronic pancreatitis

progressive inflammatory disorder with destruction of the pancreas;cells are replaced by fibrous tissue;pressure within the pancreas increases, obstructing the pancreatic and common bile ducts

hypothalamus

\-growth hormone releasing factors

\-prolactin releasing factor

\-thyrotropin releasing hormone

\-corticotropin releasing hormone

\-gonadotropin releasing hormone

\-somatostatin-inhibits GH and TSH

\-dopamine-prolactin inhibition

hyper anterior pituitary gland

gigantism, acromegaly, cushing syndrome

hypo anterior pituitary gland

dwarfism, panhypopituitarism

hyper posterior pituitary gland

SIADH

hypo posterior pituitary gland

DI

thyroid hormones

T3, T4, calcitonin

iodine

essential for the production of thyroid hormones

tsh

(from anterior pituitary) control the release of thyroid hormone

t3

more potent and rapid acting-accelerates metabolic processes (BMR, thermogenesis, cell replication, etc)

t4

homeostasis/steady state

calcitonin

secreted in response to high plasma calcium level and increases calcium deposit in bone

thyroid diagnostic tests

\-TSH

\-serum-free T4

\-T3 and T4

\-T3 resin uptake

\-thyroid antibodies

\-radioactive iodine uptake

hyperthyroidism

\-graves’ disease (most common cause)

\-thyrotoxicosis

\-autoimmune disorder

\-affects women 8x more than men

thyrotoxicosis

excessive output of thyroid hormone (thyroid storm)

hyperthyroidism clinical manifestations

\-nervousness;rapid pulse;heat intolerance;tremors;skin flushed, warm, soft and moist;exophthalmos;increase appetite;weight loss;elevated systolic BP; cardiac dysrhythmias

hypothyroidism

\-primary hypothyroidism=95% of cases

\-untreated can progress to myxedema

\
causes:

\-hashimoto’s-most common

\-atrophy

\-medications

hypothyroidism treatment

\-radioactive iodine

\-thyroidectomy

\-hormone replacement: synthroid and levothyroxine

methimazole

blocks synthesis of thyroid hormone

digitalis

can decrease effect

anticoagulants

can potentiate

antacids

can interfere with absorption

sedative

pt may need less

hypocalcemia effects

cardiac: Q-T prolongation and V-tach

\-neuro: anxiety, confusion, irritability, seizures, mental retardation (children), paresthesia, twitching, muscle spasm

\
\-bronchospasm/laryngospasm

\-tetany: trousseau and chvostek’s signs

parathormone

regulates calcium and phosphorus balance

increased parathormone

elevates blood calcium by increasing caclium absorption from kidney, intestine and bone

\
\-also lowers phosphorus level

hypercalcemia treatment

\-dietary modifications/stop supplements

\-hydration→ promote diuresis

\-loop diuretics/dialysis

\-phosphate-IV/neutraphos

\-monitor EKG and vitals

\-labs: BUN/createnine/Ca+/K+/Albumin/Digoxin

\-poss. fall precautions

\-stool softeners

hyperparathyroidism

\-may experience no symptoms

\-apathy, fatigue, muscle weakness, nausea, vomiting, constipation, hypertension, cardiac dysrhythmias

hyperparathyroidism treatment

surgical removal of abnormal parathyroid tissue, hydration therapy

hypoparathyroidism causes

\-abnormal parathyroid development

\-destruction of the parathyroid glands (surgical removal or autoimmune response)

\-vitamin d deficiency

hypoparathyroidism clinical manifestations

\-tetany

\-numbness

\-tingling in extremities

\-stiffness of hands and feet

\-bronchospasm

\-laryngeal spasm

\-carpopedal spasm

\-anxiety

\-irritability

\-depression

\-delirium

\-ECG changes