Exam 5

Question 1

What are the different types of dysphagia?

Answer 1

Achalasia: food gets stuck in the esophagus
-failure of the lower esophageal sphincter to relax due to loss of nerve innervation

Congenital atresia: developmental disorder where the upper and lower esophagus are not connected, fixed by surgical correction

Stenosis: narrowing of the esophagus, may be developmental or acquired defects

Diverticulum: undigested food becomes trapped in pouch and ferments, causing bad breath

Tumor: compression or blockage inside or outside esophagus

Question 2

What are some signs and symptoms of dysphagia?

Answer 2

pain when swallowing
inability to swallow large pieces of solids
difficulty swallowing liquids

Question 3

What are the most common causes of acute and chronic gastritis

Answer 3

gastritis caused by increased release of gastric juice and decreased mucus production

Acute Gastritis: inflammation of the stomach
Causes:
NSAIDS/Aspirin (breakdown mucus lining)
Alcohol (increase gastric juice)
Chemotherapy/Gastric Radiation (breakdown mucus barrier)

Chronic Gastritis: permanent damage to stomach wall, atrophy of gastric mucosa

-H.Pylori gastritis: most common, produces substances that neutralizes the acid pH of stomach. H. Pylori raises pH of environment, liquifies mucin layer

-Autoimmune gastritis:
body attacks w/autoantibodies against parietal cells of stomach and intrinsic factor, deficit in stomach acid secretion and vitamin B12 deficiency

Question 4

What are the signs and symptoms of gastritis? What are the treatments?

Answer 4

gastric mucosa is inflamed, red, edema, may be ulcerative/bleeding,

chronic gastritis:
causes changes to mucosa
-atrophy of gastric mucosa w/loss of secretory glands

-treated with antibiotics, histamine receptor antagonists, and proton pump inhibitors

Question 5

In which type of gastritis might you see pernicious anemia and why?

Answer 5

Pernicious anemia is often seen in chronic gastritis due to the destruction of gastric cells that produce intrinsic factor, necessary for vitamin B12 absorption.

Question 6

What is the main cause of gastric ulcer?

Answer 6

H. Pylori/ too much aspirin/NSAID

Question 7

How is a gastric ulcer treated?

Answer 7

Get rid of H. Pylori, avoiding NSAID, proton pump inhibitors, histamine receptor antagonists, antacids

Question 8

What are the two types of inflammatory bowel disease (IBD)?

Answer 8

Crohn’s disease and Ulcerative colitis.

Question 9

What are the causes and symptoms of Crohn’s disease?

Answer 9

-Affects any area from mouth to anus (digestive tract)

-Full thickness/inflammation of bowel (transmural), affects inner lining of mucosa, submucosa, and serosa, progress to shallows ulcers-narrowing of lumen may lead to complete occlusion

• leads to inability to digest/absorb foods
  -chronic diarrhea
  -fistula form
  -exacerbation/remission
• increased risk of colorectal cancer
  -can scar intestine and result in intestinal blockage

Question 10

What are the treatments for Crohn’s disease/Ulcerative colitis?

Answer 10

anti-inflammatory medications
anticholinergic medications
nutritional supplements during acute episodes
antimicrobials
surgery (ileostomy/colostomy)

Question 11

What are the causes and symptoms of ulcerative colitis?

Answer 11

inflammation of the rectum and colon, confined to mucosa
-tissue becomes edematous and ulcers develop
-tissue bleeds easily
-tissue destruction interferes w/absorption of fluid/electrolytes
-long term complication: colorectal carcinoma (colon cancer)

Question 12

What is Clostridium difficile colitis? (C-DIFF)

Answer 12

When there is a disruption in natural flora of LI. Seen in people on broad-spectrum antibiotics, where good bacteria in intestines are destroyed, allowing bad bacteria (C-DIFF) to overpopulate intestine.
-acquired by oral-fecal route
-acquisition of C. diff spores (when someone swallows them), the spores germinate(wakeup) leading to the overgrowth/toxin production
-results in binding/damaging mucosa layer, causing hemorrhage + inflammation
-antibiotic make LI susceptible of infection

Question 13

How is Clostridium difficile colitis treated?

Answer 13

Stop current antibiotic treatment, treat w/antibiotic that will kill the C-Diff
-metronidazole, vancomycin

Fecal transplant/fecal bacteriotherapy

Question 14

What are the different types of diarrhea?

Answer 14

Acute diarrhea- self limiting (go by itself), caused by infectious agent

-Noninflammatory diarrhea- caused by toxin produced by bacteria. Large volume, watery, non-bloody. cramping, bloating, nausea, vomiting. Can result in hypokalemia and dehydration.

-Inflammatory diarrhea: bacteria invading intestinal wall or toxins attach to wall and cause damage. Small volume. Mainly affects colon. Fever, bloody diarrhea

Chronic diarrhea- symptoms persist for weeks, associated with IBS, IBD, malabsorption disorders

Osmotic diarrhea: caused by hyperosmotic chyme (intestines pull water in)
-lactose intolerance

Secretory diarrhea: increased intestinal secretions or excess bile salts in SI.
-infections

Question 15

What is the difference between GERD and reflux?

Answer 15

Reflux: backward flow of stomach acid into esophagus
-short term

GERD: chronic condition due to damage or lower esophageal sphincter not closing tightly (weak/incompetent), substances leak back up
-burn 30-60 min after eating, worse when bending/lying down
-refluxate (acid) causes esophagus mucosa injury
-chronic cough/horseness
-if chronic, can lead to Barrett esophagus

Question 16

What is Barrett’s esophagus?

Answer 16

It is a type of dysplasia caused by Chronic GERD
that changes the esophagus over time. Can lead to adenocarcinoma (esophagus cancer)

Question 17

How might GERD be treated? Mechanism of Action?

Answer 17

Antacids (neutralize acid)
H2 Receptor antagonists (Hist. stim release gast. juice)
proton pump inhibitors (block release HCl)

Question 18

List the different types of vomit and what each indicates.

Answer 18

Hematemesis: vomit that looks like coffee, due to bleeding in the stomach (partially digested Hg). Presence of blood.

Yellow/green vomit; represents bile from the duodenum

Deep brown vomit; indicates contents from the lower intestine (ileum), seen in pt w/ intestinal obstruction

Frank blood in vomit; indicates issue in esophagus

Question 19

Describe the different ways blood can appear in the stool.

Answer 19

Frank blood- blood appears in surface of stool, indicates bleeding in rectal area. Appears red b/c it has not been digested and usually results from lesions in rectum/anal canal.

Melena - dark stool resulting from bleeding in the intestinal tract (transverse, ascending, descending colon), and the blood has been digested

Occult blood - hidden blood that is not visible to the eye, can be detected upon testing the stool

Question 20

Describe the pathophysiology of dumping syndrome. S/S.

Answer 20

Normally, when you chew food, it goes in your stomach and mixes with gastric juice (chyme) , very slowly gets released into Duodenum. Pyloric sphinctor relax & hyperosmotic chyme will enter and close up.

Dumping Syndrome:
-unregulated movement of chyme from stomach into SI.
-excess amount of hyperosmotic chyme dumped into SI, drawing fluid in, causing intestinal distention and increased gastric motility.
-gastric resection
-gastric bypass

S/S
cramps, nausea, diarrhea, hypovolemia, hyperglycemia followed by hypoglycemia

Question 21

Why do people with dumping syndrome develop hyperglycemia followed by hypoglycemia?

Answer 21

Due to rapid gastric emptying into the SI of hyperosmolar chyme, you become hypovolemic. When the food is dumped in the stomach it is rapidly digested and absorbed. First, the pt will go into hypervolemic state, insulin is released, 2-3h later, insulin still active hypoglycemic state b/c there is no reserved food left in the intestinal tract to replace all the glucose that was taken up into cells that have been stimulated by insulin

Question 22

S/S of hypovolemia

Answer 22

Decreased BP
Faint, weak, dizzy
Tachycardia
pallor, diaphoresis

Question 23

S/S hypoglycemia

Answer 23

weak, confused, tachycardia, pallor, diaphoresis

Question 24

What is the difference between mechanical and paralytic bowel obstruction?

Answer 24

Mechanical obstruction: A physical blockage in intestines that results in high pitched peristalsis (bowel sounds), may be absent later.
-intestinal hernias
-tumors in SI/LI
-IBD’s, like Crohn’s
-twisting of intestines (volvulus)
-telescoping of intestine (intussusception)

Paralytic obstruction: bowels stop moving. Inaudible bowel sounds.
-malfunction of nerves/muscle
-electrolyte imbalance
-gastroenteritis, appendicitis, pancreatitis,
-some drugs/meds

Question 25

What are the signs and symptoms of mechanical/paralytic bowel obstruction?

Answer 25

-vomiting deep + brown, (fluid/electrolyte losses) -fluids move to intestinal contents -gas accumulates -distention of bowel, you can crimp off blood vessels, resulting in compartment syndrome, leading to ischemia and necrosis of bowel -anaerobic bacteria produce endotoxins

Question 26

What is cirrhosis? S/S? Why does a patient develop ascites with cirrhosis ?

Answer 26

End stage of chronic liver disease. Normal liver cells are replaced by fibrous tissue. Caused by alcohol, hepatitis, non-alcohol liver disease. If a pt has hepatitis and you can remove whatever is damaging the liver, it'll heal by itself. Once you have cirrhosis the damage is irreversible. -Progressive and leads to fibrosis (scarring liver tissue), Decreasing blood and bile flow, causes liver failure These patients get Ascites (fluid in abdomen) due to low plasma proteins and increase in hepatic portal pressure, pushing fluid into the abdominal cavity. S/S -develop ascites -weight loss -weakness -bleeding

Question 27

Which of the following would you expect to see in a pt w/ cirrhosis/liver failure/ hepatitis?

Answer 27

Increased liver enzymes Decreased plasma proteins

Question 28

What causes jaundice?

Answer 28

Excess unconjugated bilirubin in the blood. It is very lipophilic and results in jaundice because unconjugated bilirubin attach to elastase in sclera and fat in the hypodermis -high levels of bilirubin in blood

Question 29

Differentiate between prehepatic, intrahepatic, and posthepatic jaundice.

Answer 29

Prehepatic jaundice: excessive destruction of RBC -seen in newborns, they take all fetal RBC w/fetal Hg and convert into adult RBC w/adult Hg & seen in pt w/hemolytic anemia -not liver's fault -since bilirubin is lipophilic, it can easily cross blood-brain barrier, and unconjugated bilirubin is deposited into brain of child (Kernicterus) Intrahepatic jaundice: patients w/ liver disease -liver fault Post hepatic jaundice: caused by obstruction of bile flow into gallbladder or duodenum -outflow problem

Question 30

What are the stages of hepatitis? S/S each stage

Answer 30

1) Preicteric/prodromal period -insidious/gradual onset w/fatigue, malaise, anorexia, nausea, muscle ache, fever/headache, elevated serum liver enzymes AST, ALT -if issue caught here and resolved, liver can heal itself 2) Icteric/jaundice period -jaundice due to bile flow obstruction, -dark urine, lots of bile -feces, lighter color, (brown color due to bile) -liver tenderness -priuritus (itching) 3) Convalescent period (postinteric) -recovery phase -reduction in s/s

Question 31

How are liver cells damaged by the hepatitis virus?

Answer 31

1) Direct action of the virus -virus directly invades lhepatocytes (liver cells) and causes damage directly. Infected hepatocytes can be destroyed as the virus replicates. Cell injury leads to inflammation and necrosis. 2) Cell mediated immune response - The IS attacks infected liver cells. Inflammation occurs as the body tries to get rid of the virus. Results in necrosis of liver cells. -The amount of enzymes in circulation indicates amount of damage done.

Question 32

What is hepatitis, its causes and s/s

Answer 32

Hepatitis is inflammation of the liver, often caused by viral infections, toxins, or autoimmune hepatitis (drug/alc induced/ idiopathic (random)) Chronic viral hepatitis leads to cirrhosis (scar liver) and liver cancer -principal cause of chronic liver disease, cirrhosis, and hepatocellular cancer in the world. -chief reason for liver transplant in adults

Question 33

What are the liver enzymes elevated in liver disease?

Answer 33

ALT - liver specific AST - found in other cells in body -------------------------------------------- GGT ALP Bilirubin -measure liver excretory function

Question 34

Which of the following liver enzymes indicate hepatitis?

Answer 34

-increased GGT, ALT, AST, ALP, bilirubin

Question 35

When someone has viral hepatitis, liver cells killed in what 2 ways

Answer 35

1) by the virus itself 2) by the IS attacking the viral infected cells

Question 36

What happens to plasma proteins in liver failure?

Answer 36

decreased plasma proteins

Question 37

Describe the pathophysiology of Acute pancreatitis; causes, s/s

Answer 37

Inflammation of the pancreas caused by autodigestion due to early activation of trypsin. Activated enzymes begin to digest pancreas cells. Severe pain, inflammation produce large volumes of serous exudate, leads to hypovolemia -enzymes like amylase and lipase will appear in blood & hypocalcemia. -Areas of dead cells undergo fat necrosis. Pancreatic tissue necrosing and calcium deposits on dead tissue (dystrophic calc) Cause; gall stones, alcohol abuse -pancreatic duct is blocked or sphinctor of oddi -alcohol prevents sphinctor of Oddi from relaxing, enzymes can't get into duodenum, back up into pancreatic duct. alcohol releases enzymes that digest both endo/exo pancreas. S/S -2/3 present -abdominal pain (severe), epigastric or LUQ -serum amylase/lipase 3x normal -pancreas swollen in abdominal imaging.

Question 38

Chronic pancreatitis

Answer 38

s/s -similar to acute, but chronic so Beta cells are destroyed, can't replace blood sugar levels and they increase. -digestive problems due to inability to deliver enzymes to duodenum -glucose control problems - damage done to islet of Langerhans -obstruction of biliary tract due to scar tissue forming & enlargement of pancreas. Cause: -alcohol/drug abuse

Question 39

What enzymes are indicative of pancreatitis?

Answer 39

Elevated levels of amylase and lipase

Question 40

Why does a patient with chronic pancreatitis develop type I diabetes?

Answer 40

bc autoimmune destruction of pancreatic beta cells, can't produce insulin. Islets of Langerhans's get destroyed. Body can't regulate glucose properly.

Question 41

What is peritonitis, s/s and causes. Chemical vs Bacterial peritonitis

Answer 41

Inflammation of the peritoneal membrane, mostly seen in pt w/ peritoneal dialysis. -Muscles of the abdominal wall tighten to protect inflamed bowel (Board-like abdomen) -Bowel sounds decrease, diaphragm and accessory muscle movements decrease, shallow breathing (affects breathing) -Pain and SNS stimulation cause the bowel to freeze in place. Chemical: ruptured gallbladder/spleen Bacterial: perforation in intestines; rupturing of appendix

Question 42

Why do patients with dumping syndrome have difficulty regulating blood glucose levels?

Answer 42

food enters the small intestine too quickly after eating. This causes sugar to be absorbed really fast, leading to a spike in blood glucose (hyperglycemia). In response, the pancreas releases a large amount of insulin, which drops the blood sugar too low later on — causing hypoglycemia about 2–3 hours after a meal. Since the food moves through so fast, there's no backup nutrition left to keep the blood sugar stable, which makes it hard to maintain normal glucose levels.

Question 43

What are the most common causes of endocrine disorders?

Answer 43

-Adenomas (benign tumors) - either secrete hormone or destroy endocrine glands -Congenital defects -Hyperplasia/atrophy of endocrine gland -Infection -Abnormal immune response -Vascular problems

Question 44

What is the difference between gigantism and acromegaly?

Answer 44

Gigantism: excess GH before fusion of epiphyseal plates before puberty. -caused by pituitary-secreting tumor -If a pt has gigantism and issue isn't resolved before they go through puberty, they will develop acromegaly & have both gigantism and acromegaly. -excess skeletal growth Acromegaly: GH excess after fusion of epiphyseal plates, after puberty. -pit-sec tumor + fusion ep. plates = acromegaly -exaggerated growth at ends of extremities

Question 45

What is hypothyroidism? what are its s/s and is it treated.

Answer 45

thyroid gland doesn't produce enough thyroid hormones. It can be congenital or acquired. -Hashimoto thyroiditis -thyroidectomy S/S Slow metabolism Weight gain w/loss of appetite Cold intolerant Bradycardia Muscle weakness Lethargy DECREASED T3/t4, TSH levels depend on where disorder originates, thyroid gland (primary) pituitary (2nd)

Question 46

How might a patient develop hypothyroidism?

Answer 46

Lack of Iodine; t3/t4 not made, TRH and TSH continue to be made, increased TSH causes hyperplasia/hypertrophy in thyroid gland and create a goiter. Thyroid Hormone is essential for normal growth and brain development. If no TH, brain can't develop, If congenital 🡪 mental retardation and impaired physical growth 🡪 cretinism (baby born w/little to no TH). -TH is needed for maturation of the digestive(hepatic) system. -The liver can't conjugate bilirubin properly, so unconjugated bilirubin builds up in the blood → leads to jaundice & kernicterus (bili in brain) Primary hypothyroidism: thyroidectomy or damage to gland by radiation, drugs like lithium/anti-thyroid drugs, or autoimmune response. -Myexdema; form of hypo that causes nonpitted edema. If life threatening, decreases bloodflow in brain and causes myxedematous coma, usually triggered by another issue like climate-induce hypothermia, infection, other systemic infection, or drug therapy.

Question 47

How is hypothyroidism treated?

Answer 47

Hormone replacement therapy (Synthroid, Levothyroxine) -If treating hyperthyroidism w/ I- or surgery to remove the thyroid gland, they will go from hyperthyroidism to hypothyroidism

Question 48

What is the most common cause of hypothyroidism?

Answer 48

Hashimoto's thyroiditis (body makes antibodies that destroy thyroid gland) removing the thyroid gland

Question 49

What is the difference between growth hormone and IGF-1?

Answer 49

Growth hormone is released by the pituitary gland, it stimulates the liver to make IGF-1, causing growth in bones, muscles, and tissues.

Question 50

What is the direct function of growth hormone?

Answer 50

increase the breakdown of lipids increase use of FA decrease glucose use increase serum glucose

Question 51

What is hyperthyroidism? S/S

Answer 51

Hyperactivity of thyroid gland produces too much thyroid hormone. -'thyrotoxicosis' -caused by Grave's disease & thyroid tumors -Type 2 hypersensitivity reaction -TSH- Secreting tumor of thyroid gland, increased T3/T4, enlarged thyroid gland -diffuse goiter, multinodular goiter S/S Hypermetabolism Weight loss Heat intolerant Tachycardia Exopthalmos T3/T4 increase TSH levels depend on where disorder originates, thyroid gland (primary) pituitary (2nd)

Question 52

How might a patient develop hyperthyroidism?

Answer 52

Graves' disease - autoimmune disease where body makes antibodies that bind to TSH receptor. Triad of hyperthyroidism, goiter, and ophthalmopathy/exophthalmos thyroid nodules - hypertrophy due to excess stimulation of TSH excessive iodine intake.

Question 53

How is hyperthyroidism treated?

Answer 53

-Give meds to block synthesis (antithyroid drugs), block release (iodides), block t4 into t3 conversion, beta blocker -Give radioactive I- (thy gland takes radioactive I-, kills cells of thyroid gland). -Isolate pt on I-

Question 54

What is the most common cause of hyperthyroidism?

Answer 54

Graves' disease.

Question 55

What is a goiter?

Answer 55

A goiter is an enlargement of the thyroid gland, high TSH

Question 56

What is a thyroid storm? S/S? Treatment?

Answer 56

Extreme case of hyperthyroidism. Seen in undiagnosed pt or pt who have not received adequate treatment. -Caused by physiological stress, infection, diabetic ketoacidosis, physical/emotional trauma, manipulation of hyperactive gland during thyroidectomy S/S very high fever (104-106) extreme tachycardia (>140) CHF, Angina, agitation delirium, confusion Treatment peripheral cooling w/out shivering - to cool the temp, metabolism increases, and waste product of metabolism is heat beta blocker to slow heartrate glucose electrolytes - monitor Na+, K+

Question 57

What is the difference between Addison’s disease and Cushing’s syndrome?

Answer 57

Addison's (Primary adrenal insufficiency) - deficit in cortisol/aldosterone -adrenal cortical insufficiency -all layers of adrenal cortex destroyed -caused by autoimmune or infections -hyponatremia, hyperkalemia Acute adrenal crisis: medical emergency caused by lack of cortisol S/S: -decreased blood glucose - low cortisol, cortisol is a glucocorticoid that will increase glucose -poor stress response - low cortisol = low stress response -low serum sodium, high potassium, hypoaldosteronism -low blood volume - low on aldo, need aldo to keep blood vol. up, low BP -hypotension - low Na+2, low water in blood -hyperpigmentation - low cortisol so increased ACTH + MSH Cushing's - excess cortisol -pituitary form due to excess ACTH -adrenal form due to adrenal tumor -would see hypernatremia and hypokalemia Ectopic Cushing: ectopic cells not making ACTH, not pituitary gland Iatrogenic Cushing: pharmalogical prep of glucocorticoids S/S; physical features of obesity -moon face -heavy trunk w/ fat at back of neck (buffalo hump) -muscle wasting in limbs -osteoporosis -suppressed immune response, increasing risk of infection -hyperglycemia

Question 58

What electrolyte imbalances might you expect to see in Addison’s disease?

Answer 58

hyponatremia and hyperkalemia.

Question 59

What electrolyte imbalances might you expect to see in Cushing’s syndrome?

Answer 59

hypernatremia and hypokalemia.

Question 60

What is the difference between type I and type II diabetes?

Answer 60

Type 1: autoimmune destruction of pancreatic beta cells -IS attack beta cells in Islet of Langerhans -preadolescent -family history of type 1/ family history of autoimmune diseases -thin body weight, low plasma insulin, -autoantibody present Treat: insulin replacement -frequently hypoglycemic or ketoacidosis (no insulin so body use fat for energy) Type 2: insulin resistance and a relative insulin deficiency -most common (90-95%) -relative insulin deficit -no autoantibody present -present in immediate family (if parents obese, children more likely to be obese) -central obesity -decreased or normal plasma insulin. -insulin levels not efficient to stimulate receptors Treat: Diet and oral hypoglycemic agents. If those fail then insulin replacement -infrequent hypoglycemia or ketoacidosis

Question 61

45) As it relates to diabetes what is glycosylate hemoglobin or A1C levels, what is it and how is it

Answer 61

A1C levels reflect average blood glucose levels over the past 3-4 months and are used to diagnose and monitor diabetes.

Question 62

What are the criteria used to diagnose diabetes?

Answer 62

Fasting glucose (minimum 8hr fast) > OR =126 mg/dL Drawback: 1 time measurement Oral glucose tolerance test - how fast glucose load is removed from the blood Drawback: 1 time measurement -> or = 200mg/dL after 2 hrs A1C levels: glucose covalently bonded to hG -Drawback: long term regulation of glucose (3-4 months) -> or = 6.5%

Question 63

Hypoglycemia - causes, s/s, treatment

Answer 63

Hypoglycemia: abnormally low blood sugar. 3 ways a pt can get hypoglycemia Causes -inject self w/ too much insulin (error in dosage) -inject self w/insulin, then not eating (vomit/skip meal) -excess exercise -decreased insulin after stressful situations SS -related to Altered brain activity; headache, difficulty problem solving, poor concentration, slurred speech, lack of coordination, staggered gait, seizures, coma -related to activation of SNS; increased hunger, anxiety, tachycardia, sweating, cool/moist skin Treatment -if conscious, give something sweet, give glucose in concentrated form (in and outside hospitals) -if unconscious or unable to swallow, check for a glucagon pen (IM/SQ), give IV glucose

Question 64

Ketoacidosis, s/s, treatment

Answer 64

If the body can't use glucose as it's energy source, it goes to the next macronutrient (Fatty acids). One of the metabolic breakdown products of incomplete fat/lipid metabolism are ketoacids. They go into metabolic acidosis. -may start w/ infection or stress where the demand for insulin in body increases CAUSE: error in dosing (not giving enough insulin) diabulimia -intentionally reducing insulin intake Glucose can't enter the cells. The body starts breaking down fats and proteins. Metabolism of fats leads to the production of ketones (acidic). Buildup of ketones can cause ketoacidosis (metab. acidosis) occurs because bicarbonate decreases. S/S -increased RR (Kussmaul respirations) -breath smells like ketones - sweet -severe hyperglycemia (>250mg/dL), leads to osmotic diuresis -lethargy -decreased responsiveness -low serum bicarbonate (below 22) -low arterial pH (below 7.3) -positive urine for ketones and glucose, -electrolyte imbalances (low Na, increased K), low bicarb Treatment -give insulin to get glucose in cells, may have simultaneously give small doses of glucose IV or give IV fluids w/glucose. -Improve circulatory volume and tissue perfusion, decrease blood glucose and correct acidosis + electrolyte imbalances. -Mainly seen in type 1 diabetes, but also in type 2 if put under extra stress, increasing the bodies demand for insulin.

Question 65

What is hyperglycemic hyperosmolar state? (HHS)

Answer 65

Most frequently seen in type II diabetics and is characterized by -hyperglycemic state ( >600mg/dL) -plasma hyperosmolarity (>320 mOsm/L) -dehydration -absence of ketosis -depression of CNS cause: partial or relative insulin deificiency, causing reduce use of glucose and increased use of insulin. Massive glycosuria and massive osmotic diuresis, causing polyuria and leading to dehydration. Renal insufficiency occurs decreasing kidney's ability to excrete glucose; leading to hyperosmolarity (high conc. of solutes in blood). Water gets pulled out of cells, causing cellular dehydration (weak, excess thirst, difficulty speaking/swallowing, abnormal Babinski reflex) Treatment -insulin therapy to reduce hyperglycemic state -care must be taken as water moves back into brain cells -must treat hypokalemia -primarily seen in type 2 diabetes

Question 66

What type of Babinski reflex would you see in a pt w/HHS who has damage to their brain?

Answer 66

+ Babinski reflex (toes flare up/out)

Question 67

What are some acute complications of diabetes?

Answer 67

diabetic ketoacidosis & hypoglycemia

Question 68

What are some chronic complications of diabetes? how does each negatively impact the patient;

Answer 68

depends on if it involves big or small blood vessels. Big vessels/macroangiopathy: atherosclerosis, leads to -stroke, heart disease, HTN, PVD, Foot problems -decreased blood flow due to macroangiopathy, decreased tissue resistance, lead to gangrene. Small vessels/microangiopathy basement membrane of arteries get thick and hard, obstruction and rupturing of capillaries and small arteries, lead to necrosis -diabetic eye disease (retinopathy/cataracts) - degenerative problem caused by abnormal metabolism of glucose, accumulation of water in lenses -renal disease -neuropathy - diminished perception (vibration, pain, temp. Hypersensitivity, tingling/burning hands and feet -foot problems

Question 69

What are the three P’s of diabetes? What causes each?

Answer 69

polyuria - excess urine -Glucose in the urine exerts an osmotic pressure on the filtrate resulting in large volumes of urine w/ loss of fluid and electrolytes from body tissue polydipsia - excess thirst - fluid loss through the urine and high blood glucose levels draws fluid from cells causes dehydration, causes thirst polyphagia - excess eating (lack of glucose entering cells, constant hunger) lack of nutrients entering cells stimulates appetite

Question 70

What are the 5 ways oral hypoglycemics work?

Answer 70

1) decrease glucose output by liver 2) decrease glucose absorption by gut 3) increase insulin secretion by B-cells of pancreas 4) increase insulin sensitivity of target cells 5) increase glucose excretion in urine, decreased ability of kidney to reabsorb glucose

Question 71

What is metabolic syndrome? S/S?

Answer 71

Metabolic syndrome is a cluster of conditions that occur together, increase the risk of heart disease, stroke, and type 2 diabetes. -Hyperglycemia -Central obesity/intra-abdominal obesity\ -increased blood triglyceride levels -decreased HDL -increase bp, -decreased fibrinolysis; inhibit tPA -microvascular diseases like cad, pad

Question 72

Why might a diabetic with Cushing Syndrome have difficulty regulating blood glucose levels?

Answer 72

Cushing Syndrome causes an overproduction of cortisol, and cortisol increases blood sugar. -Cortisol affects the blood sugar by increasing glucose production, makes body more resistant to insulin, and inhibits glucose uptake in cells. In a diabetic, they already struggle with using/producing insulin. Now with excess cortisol, their body makes more sugar & responds poorly to insulin, causing hyperglycemia.

Question 73

How does insulin lower blood glucose levels; what cells types do not require insulin to take up glucose

Answer 73

Insulin stimulates uptake, use, and storage of glucose by cells. -turns extra sugar into glycogen (glycogenesis) -turns extra sugar into fat (lipogenesis) -protein synthesis (builds proteins) -needed for g+d in children Insulin inhibits glycogenesis, lipolysis, and gluconeogenesis. Cells not required insulin to take up glucose -Glucose transporter in kidneys -Neurons and skeletal muscle

Question 74

What is a hiatal hernia? What are the different types? s/s

Answer 74

When the stomach pertrudes through the esophageal hiatus, the region where the esophagus passes through the diaphragm. Axial hernia: bulge all around Paraoesophageal hernia: bulge on one side, affects lungs ability to inflate.

Question 75

What is diverticular disease? S/S?

Answer 75

Divaticulosis: pouches form in the wall of the colon, usually sigmoid colon. Most people don't have symptoms, overtime, if the pockets get inflamed/infected it is called diverticulitis. -S/S -diarrhea -cramping -abdominal pain -no fever/ no other sign of infection

Question 76

What is appendicitis? causes? s/s?

Answer 76

Appendicitis is the inflammation of the appendix, abrupt onset. The appendix can get inflamed if outflow of appendix is blocked by -gallstone, or appendix twists on itself, or -fecalith (very hard piece of stool, bacteria divide and produce gas, can't enter secum because its blocked, increasing pressure of the appendix, results in necrosis/gangrene (severe) S/S -epigastric/LRQ pain -fluid buildup, microbes proliferate -appendix wall inflamed, purulent exudate forms