Exam 2

GI bleed

GI bleed

Upper 

• 85% of bleeds 

• Esophagus, stomach, duodenum 

• Etiology 

  • Ulcer 

  • Esophageal varices 

  • Liver damage – blood backs up into portal vein and then into esophagus 

Lower 

• Jejunum, ileum, large intestine 

• Etiology 

  • IBS (irritable bowel syndrome) 

  • Hemorrhoids 

  • UC 

  • Chrons 

GI bleed manifestations

Characteristics determine activity 

• Bright blood is happening in the moment and is not passed through the stomach 

• Coffee ground emesis 

  • blood mixed with stomach acids

Hematemesis 

• Blood in vomit 

• Described as bright red or as coffee ground

Melena 

• Bright red blood in stool 

  • Low in GI tract 

• Tarry 

  • Older less severe bleed or traveled through the tract 

• Occult blood – hidden in the stool

GERD

• Lack of pressure -> relaxation of gastroesophageal sphincter 

Etiology 

• Smoking 

• Chocolate 

• ETOH 

• Fatty foods 

• Caffeine 

• Meds 

• Pregnancy 

Manifestation 

• Heart burn 

  • An hour after eating and/or laying down 

• Chest pain 

  • Can mimic MI (Myocardial Infarction) 

• Feeling like cannot swallow or stuck in throat 

• Ulcerations 

hiatal hernia

• Present to some degree in 50% of the population 

• Portion of the stomach is moving through diaphragm into the esophagus or next to the esophagus 

Manifestations 

• Heartburn 

• Dysphagia 

• Epigastric pain 

• GERD 

Etiology 

• Paraesophageal hernia if it twists can lead to necrosis 

• Mallory Weiss tear 

• Tear in esophagus from prolonged vomiting 

• ETOH 

gastritis

• Inflammation of gastric mucosa 

Etiology 

• Endotoxin 

• Caffeine 

• ETOH 

• NSAID 

• Aspirin 

  • Blocks prostaglandins 

Manifestations 

• Mild - Gastric pain 

• Severe - Vomiting 

• Severe - Bleeding 

peptic ulcer

Etiology 

• ETOH 

• Aspirin, NSAIDS 

• Bile acids 

• Helicobacter pylori 

Mechanisms 

• Decrease mucus production and prostaglandin deficiency 

Manifestation 

• Vague abdominal pain to life-threatening hemorrhage 

• Pain usually burning, cramping, mid epigastric area 

• Perforation of gastric ulcer can lead to contents in the peritoneum 

• Decreased hematocrit

Chrons disease

• Recurrent inflammation affecting any portion of the GI tract 

• Affecting LI and SI 

• 15-35 yrs. old 

Etiology and pathogenesis 

• Possible autoimmune problem – tumor necrosis factor 

• Lesion in bowel 

• Thickening of bowel and decreased flexibility 

• All layers of the gut 

• Genetic/hereditary component 

Mechanism 

• Lesions develop in the bowel 

• Occur in patchy areas 

• 30% in LI 

• 40% in SI 

• 30% other 

chrons manifestations and complications

Manifestations 

• Periods of exacerbation and remission 

  • Alternate between diarrhea and constipation 

• Oral lesions 

• Abdominal pain 

• Equal urgency and frequency 

• Weight loss – malabsorption 

• Increased risk of intestinal cancer 

Complications 

• Fistula development from fibrosis 

• Skin or vaginal 

• Fistula between rectum and vagina 

• Intestinal obstruction 

• Abdominal and peritoneal abscess 

ulcerative colitis

• Inflammatory condition of the colon 

• Incidence highest in 20s and 30s 

• Increase risk of developing colon cancer

Etiology and pathogenesis 

• Lesions become necrotic and can ulcerate 

• Only occurs in rectum and colon 

• Lesions are continuous unlike chrons 

UC manifestations and complications

Manifestation 

• Decreased appetite (anorexia) 

• Fatigue 

• Frequent stool – diarrhea's 

• Bloody stool 

• Mucousy stool 

• Fever severe abdominal pain 

Complication 

• Colon cancer 

• Arthritis 

diverticular disease

• cannot eat popcorn, nuts, seeds 

• most prevalent in developed worked bc of lack of fiber 

• Increased pressure can be caused by lack of activity 

Etiology 

• Mucosal layer herniates through muscular layer 

• Often multiple diverticula 

• Occurs most in sigmoid colon 

• Disease is most prevalent in developed world due to lack of fiber in the diet 

Prevention 

• Increase fiber 20-35g of fiber 

• Increase hydration 

diverticulitis

Mechanism 

• Inflammation of diverticulum with small ulcerations 

Manifestation 

• Increased WBC 

• Nausea 

• Vomiting 

• fever 

Complications 

• Peritonitis 

• Bowel obstruction 

• Hemorrhages 

• Fistula formation 

colorectal cancer

• Not every polyp is cancerous 

• Can be lethal 

• Symptoms occur in late stages 

  • Why it is so lethal 

Etiology  

• Genetic and environmental causes 

• Familial adenomatous polyposis 

  • Genetic 

• Hereditary non-polypuosis colon cancer 

  • No polyps 

• Environmental 

  • Low-fiber high fat 

  • Dietary fat intake – increase synthesis of bile acids 

  • Inadequate intake of vitamins A, C, and E 

  • Cauliflower cabbage, Brussels sprouts 

colorectal cancer manifestations

• Bleeding – significant early symptom 

• Change in bowel habits 

• Diarrhea 

• Constipation 

• Urgency or incomplete emptying of bowel 

• Pain is a late symptom 

IBS (irritable bowel syndrome)

• Chronic and recurrent intestinal symptoms 

• 15-20% of the population 

• Most do not seek medical attention 

Etiology 

• Stress 

• Hyperactivity of the bowel 

Manifestations 

• Symptoms  

  • Abdominal pain 

  • Complaints of flatus 

  • bloatedness 

  • Nausea 

  • Anorexia 

  • Anxiety 

  • Depression 

  • Vomiting 

• Signs  

  • Changes in frequency and consistency of stool 

  • Symptoms for at least 3 months to get dx

hepatitis A

Etiology 

• Virus 

• Single stranded RNA Virus 

• Incubation period of 2-6 weeks 

• Hepatocytes are sole site of replication 

• Fecal – oral route of transmission 

  • Breastmilk, water, shellfish 

Symptoms 

• Fever 

• Malaise 

• Nausea & anorexia 

• Jaundice 

• Tea colored urine & clay-colored stools 

Once disease resolves – develop antibodies and will not return 

hepatitis B

Etiology 

• Double-stranded – DNA virus binds to hepatocytes 

Transmission 

• Blood and bodily fluids (saliva and semen) 

Prophylaxis 

• Hep B immune globulin 

• Hep B vaccine 

Groups at risk 

• Healthcare providers 

• Sexually active heterosexuals or homosexuals 

• IV drug abusers 

• Autoimmune response – inflammation of the liver 

• This leads to damage and destruction of bile cannula 

hepatitis B and C manifestations

Manifestations 

• Do not occur for 2-3 months after exposure  

• Fulminant hepatitis  

  • Rare syndrome  

  • Rapid (days or weeks) massive necrosis of liver parenchyma and atrophy of liver 

  • High mortality 

• Fatigue 

• Malaise 

• Anorexia 

• Headache 

• RUQ pain 

• Decreases in liver function tests

carrier state Hep B

• continue to harbor the virus, no symptoms, are contagious 

• Anti-HBc – antibody to core antigen- means you had exposure to the disease 

• Patients do not develop antibody to the surface antigen. 

• No Anti-HBs

chronic hepatitis

• may or may not have symptoms 

• Later stages develop liver failure 

• Positive surface antigen  

• Virus is still replicating  

• No antibodies

hepatitis C

• Chronic hepatitis 

• Single stranded RNA Virus 

• Also transmitted through blood and bodily fluids 

• No vaccine for Hepatitis C 

• 80% of patients will go on to be carriers 

• Progressive fibrosis leads to cirrhosis and end stage liver disease 

• Higher incidence of cancer

complications of cirrhosis

o portal hypertension
o splenomegaly
o ascites
o hepatorenal syndrome
o hepatic encephalopathy
o esophageal varices

portal hypertension

increased pressure within the portal venous system

can cause:

• Ascites

• Splenomegaly

esophageal varices

• Backup in veins of esophagus 

• Low pressure system becomes high pressure 

• Causes weakening and out-punching of esophageal veins 

• Life threatening 

ascites

• accumulation of fluid within the peritoneal cavity 

spelomegaly

• due to shunting of blood into the splenic vein

hepatic encephalopathy

• central nervous system manifestations 

• Toxins cross blood brain barrier 

Symptoms 

• asterixis - flapping tremor 

• loss of memory 

• personality changes 

• impaired speech 

• Coma 

Lactralose 

• Binds to ammonia and excreted through feces 

hepatorenal syndrome

a multiorgan condition affecting the kidneys and the liver

• Possibly due to decreased renal blood flow 

• increased creatinine 

• increased BUN 

• decreased urine output 

cholelithiasis

• development of gallstones 

Etiology

• high cholesterol in bile 

Mechanism

• development of cholesterol stones 

Manifestation

• may be asymptomatic

adrenal axis

• Stress stimulates hypothalamus to release CRH 

• Stimulates anterior pituitary to release ACTH  

• Stimulates adrenal glands to release glucocorticoids and mineralocorticoids 

• Glucocorticoids - cortisol 

• Mineralcorticoids – ADH – affects sodium and water 

thyroid axis

• TRH – thyroid releasing hormone stimulates TSH from anterior pituitary hormone 

• Stimulates release of T3 or thyroxine (T4) from thyroid  

• With hypothyroidism there is negative feedback mechanism bc T3 and T4 are decreased so TRH and TSH increase (tertiary problem) 

primary disorder

• when the end organ is not able to put out the hormone 

  • examples e.g., thyroidectomy or adrenalectomy 

  • hyper/hypothyroidism - problem with thyroid gland TRH and TSH will decrease 

  • hypothyroidism - problem with

secondary disorder

• when the hypothalamus or pituitary are unable to put out hormone 

  • example e.g., removal of the pituitary gland 

  • secondary hyper/hypothyroidism - problem with the pituitary or hypothalamus

    • TSH and TH will increase 

    • TRH will decrease 

Hypothalamic pituitary regulation 

Hypothalamus causes release of hormone → pituitary releases hormone → stimulates the gland to release hormone that targets cells

antiduretic hormone

• arginine vasopressin released from the posterior pituitary in response to increased osmolality sensed in the supraoptic nuclei of the hypothalamus 

• release also stimulated if plasma volume low 

• sensed in the aortic and carotid arch, and left atrium target organ distal tubule of the kidney collecting duct 

• Released from posterior pituitary 

  • Produced in hypothalamus 

• Does not travel via portal system like with anterior pituitary  

Causes release 

• Plasma osmolarity 

  • How concentrated blood is  

  • 280-295 mOs/kg 

• Increase = release of ADH 

  • Also increase in thirst 

thyroid hormone

• Helps with metabolic rate 

• HR and contractility are enhanced 

• Potentiates (makes the more effective) norepinephrine and epinephrine 

• Growth and development in children 

• Metabolic Rate - increase in BMR by 60 to 100% by large amounts of thyroxine secretion 

• Cardiovascular Function - heart rate and contractility are enhanced 

• Gastrointestinal Function - increased appetite 

• Neuromuscular Effects 

  • increased levels, muscles react more vigorously 

  • decreased levels, muscles are more sluggish 

diabetes insipidus

• insufficiency of ADH 

Etiology 

• neurogenic - inadequate production problems with synthesis, transport, release due to: 

  •  tumors 

  • hypophysectomy 

  • aneurysms 

  • thrombosis 

  • infections 

  • immunologic disorders 

  • commonly head injury 

• nephrogenic - inadequate response 

  • genetic 

  • some drugs damage the renal tubules 

  • pyelonephritis 

  • polycystic disease 

  • general anesthetics 

  • lithium carbonate 

diabetes insipidus manifestations

• low urine specific gravity 1.000 to 1.005 

• low urine osmolality 

  • Less concentrated and more watery 

• polyuria 

  • 1/2 cases 4 to 8 L/day 

  • 1/4 of cases 8 to 12 L/day 

• dehydration unless fluid replaced 

• Increased blood osmolality 

SIADH (Syndrome of Inappropriate Antidiuretic Hormone Secretion)

• Genetic derepressing 

  • Functions are unlocked 

  • Production of ADH 

  • Cancer cells begin to produce ADH 

    • No regulation 

  • Become hyponatremic 

    • Decrease in serum sodium and serum osmolality 

    • Changes in LOC 

    • Can see seizure activity 

Etiology 

• ectopic tumor cells 

• oat cell adenocarcinoma of the lung 

• carcinoma of the duodenum, pancreas, etc. 

Mechanism 

• water retention 

• expansion of intravascular volume 

SIADH manifestations

Signs 

• hyponatremia - dilutional 

• hypo osmolality - dilutional 

• urine hyperosmolality - concentrated 

Symptoms 

• thirst 

• impaired taste 

• GI symptoms

  • vomiting

  • abdominal cramps 

• Neuro symptoms 

  • confusion 

    • lethargy 

  • muscle twitching 

  • Convulsions 

hypothyroidism

Etiology 

• lymphocytic thyroiditis most common 

• thyroidectomy 

• secondary hypothyroidism 

Manifestations of hypothyroidism 

• Weakness – most common 

• fatigue 

• tendency to gain weight 

• cold intolerance 

• decreased gastric motility 

• mental dullness 

• lethargy 

• impaired memory 

• Goiter  

  • Not enough iodine  

  • Still increases in size because it is trying to release T3 and T4

hyperthyroidism

Etiology & Mechanisms 

• graves' disease – most common 

• Antibodies produced that bind for TSH in thyroid 

• Cause release of T3 and T4 

• adenoma of the thyroid 

•  OD thyroid hormone 

myxedema coma

• coma 

• hypothermia 

• cardiovascular collapse 

• hypoglycemia 

• hyponatremia 

hyperthyroidism manifestations

• hypermetabolic state – most common 

• Nervousness 

• Goiter 

• Increases due to overactivity 

• Exophthalmos 

  • Buildup of mucous membrane behind the eye 

• irritability 

• fatigue

• weight loss 

• large appetite 

• tachycardia 

• palpitations 

• shortness of breath 

• Sweating 

• Loss of menstrual cycle 

• Oligomenorrhea 

• Increase in temperature

addison’s disease (primary adrenal insufficiency)

Etiology 

• Autoimmune - 75% of cases 

• Many other rare causes 

• fungal infection 

• viral infections 

• metastatic cancer 

• adrenal hemorrhage 

• genetic predisposition 

Mechanism 

• 90% of adrenal gland destroyed before signs show up 

addison’s manifestations

• insufficient mineralocorticoid effects – most common 

• urinary losses of sodium, chloride, water, decreased excretion of potassium 

• orthostatic hypotension 

• dehydration 

• weakness 

• fatigue 

• hyperkalemia 

• hyponatremia 

• insufficient glucocorticoid effects 

• poor tolerance to stress 

• hypoglycemia 

• lethargy 

• weakness 

• Bronze color to skin 

  • Produce too many melanocytes stimulating hormones 

cushing’s

Etiology 

• administration of corticosteroids – most common 

  • prednisone 

• inappropriate production of ACTH from ectopic tumors 

• inappropriate production of CRH from ectopic tumors 

• adrenal tumors 

• pituitary tumors producing too much ACTH 

cushing’s manifestations

Manifestations 

• Obesity - extremities are unaffected altered fat metabolism – most common 

• Skin - loss of subcutaneous fat skin becomes thinner 

  • Poor wound healing 

• Musculoskeletal system - increased bone resorption causes osteoporosis, muscle wasting 

• Cardiovascular system - HTN 

• Gastrointestinal system - increased gastric acid secretion

• Sex Characteristics - 

  • menstrual irregularities 

  • increased facial hair in females 

  • decreased libido in men and women 

• Eyes - increased ocular pressure 

• Glucose Intolerance – insulin resistance, increased gluconeogenesis 

• Psychological Changes - irritability, emotional lability, depression, paranoia 

• Thinning of hair 

• Facial flush 

• Pendulous abdomen 

• Easy bruising 

• Increased blood glucose 

  • Insulin resistance 

• Osteoporosis  

secondary adrenal insufficiency

• destruction of pituitary 

Etiology 

• pituitary tumors 

• pituitary infarctions 

• trauma 

• radiation 

• surgery

Manifestations 

• Insufficient glucocorticoid effects 

• poor tolerance to stress, hypotension 

• hypoglycemia 

• lethargy 

• Weakness

parathyroid hormone

• responsive to ionized calcium 

• produces parathyroid hormone 

• Helps reabsorb calcium in the kidneys and gut 

• Helps osteoclasts to break down bone and increase calcium levels

hypoparathyroidism

Etiology 

•  incidental surgical removal during thyroidectomy 

Signs - manifestations related to hypocalcemia 

• increased neuromuscular excitability 

• Seizures 

• Abnormal EKG (due to lack of calcium) 

• Trousseau's - carpal pedal spasm 

Symptoms 

• tingling in the hands 

hyperparathyroidism

• Seen more than hypoparathyroidism 

Etiology  

• Idiopathic – do not know why 

• Will remove part of parathyroid glands to treat it 

Manifestations 

• pathologic fractures 

• increased calcium in blood 

• Can lead to calcium stones in the kidneys 

• Osteopenia 

• Pathologic fractures 

• excretion of phosphate 

glucagon

• Alpha cells of the pancreas 

• Released with decreased glucose levels 

• Stimulates glycogenolysis (glycogen -> glucose) & gluconeogenesis (breakdown of amino acids to form glucose) 

insulin

• Beta cells of the pancreas 

• Released with increases in glucose 

• Promotes movement of glucose into cells 

• Helps build fat stores 

• Decreases gluconeogenesis

type 1 DM

Etiology

• Genetic factors 

• Autoimmunity 

  • Pancreatic beta cells destroyed by T-lymphocytes 

    • Results in insulin deficiency and eventually dependence 

• Environmental factors 

Mechanisms

• Develops during childhood or young adults 

• Begins asymptomatic 

• Insulin dependent

Manifestations

• Polydipsia 

  • Very thirsty 

  • So much sugar in bloodstream 

  • Increasing amount of solutes in the bloodstream creates a state of dehydration 

• Polyphagia 

  • Increased hunger 

  • Glucose cannot enter cells due to decrease in insulin 

  • Body is starving 

• Polyuria 

  • Kidneys are trying to dump out excess glucose in urine 

type 2 DM

Etiology

• Genetic and Environmental Factors 

  • 60% of individuals with this type of DM have a sibling or parent with Type II DM 

• Glucose Metabolism 

  • Hyperglycemic; sufficient insulin levels, insufficient insulin receptors 

Mechanism

• Non-Insulin Dependent 

  • Failure of beta cells to keep up with insulin production 

  • Insufficient insulin production by beta cells 

  • Insulin resistance secondary to obesity – can reverse with weight loss 

  • Adequate insulin production decreased sensitivity 

  • May initially be asymptomatic 

diabetic ketoacidosis

• Usually type 1 DM 

• Lack of insulin -> fatty acid mobilization -> ketone bodies - > metabolic acidosis 

• CBG 400-600 mg/dl 

• Hyperglycemia – osmotic diuresis 

• Glucosuria (glucose in urine), polyuria (excessive urination), dehydration, hypokalemia (low levels of potassium) 

• Potassium moves inside the cell with insulin 

• With no insulin it stays in the blood stream and is unused 

DKA manifestations

Manifestations

• fruity breath 

• Tachypnea 

• Polyuria 

• Polydipsia 

• N/V 

• Fatigue 

• Dehydration 

• coma 

HHNK (hyperglycemic hyperosmolar nonketotic coma)

• Usually, T2DM 

• Plasma glucose > 600 

  • Higher than DKA 

• No ketone bodies 

• Osmotic diuresis -> dehydration 

• most frequently in type II NIDDM individuals 

  • Type 2 non-insulin dependent diabetes mellitus  

• mortality rate 40 to 70 % 

Manifestations 

• Decreased LOC 

• Seizure 

• Hemiparesis 

• One sided weakness 

• Aphasia 

• Muscle fasciculations (twitches) 

• Polyuria 

• Dehydration 

• Hyperthermia 

diabetic neuropathy

Etiology 

• vessel ischemia to nerve 

• demyelination of the Schwann cell 

Manifestations 

• loss of feeling 

• loss of touch 

• position sense lost 

• impaired temperature and pain sensation 

• impotence 

diabetic retinopathy

• leakage of plasma from the vessels 

• fibrotic changes and new blood vessels develop in the retina due to ischemia

nephropathy

Causes CKD (chronic kidney disease) or end stage renal disease 

sleep stages

non-REM

• stage 1-4

REM sleep

sleep deprivation

Manifestations

• Drowsiness

• Inability to concentrate

• Impaired memory

• Reduced physical strength

• Diminished ability to fight off infections

• Hallucinations

• Severe mood swings

sleep changes across lifespan

• sleep stage 50-60 minutes in infants 

  • Will sleep a lot 

  • 80% is REM sleep 

  • Newborns sleep 17-24 hours a day 

  • Age 2 – REM 30-35% 

  • Infants in 6 months 14-15 hours 

• sleep stage 90 minutes long in the adult 

  • decreased sleep requirement over time 

• stage 4 sleep is absent in individuals 70 years of age or older 

  • Sleep in elderly is related to dementia 

  • Easier to wake up bc no stage 4 

physiologic changes in sleep

• cough reflex diminished 

• decreased clearance of respiratory secretions 

• decreased swallowing and esophageal motility 

• decreased glomerular filtration rate 

• increased aldosterone production 

• REM 

  • serotonin needed for priming of REM sleep 

  • loss of muscle tone 

  • loss of ability to thermoregulate 

  • eye movements 

  • Rapid irregular respirations 

fever manifestations

Behavioral

• Put on clothes 

• Put on blankets 

Experiential

• Increased amount of slow sleep 

• CV 

  • HR increase 

  • 10% rise in metabolic rate per 1 C degree rise 

  • Increased O2 consumption because metabolic rate 

• Immune system function is enhanced 

  • Fever is treated when it gets to hyperthermia because it can damage CNS 

  • Treat pregnant moms 

  • People w cardiac or pulmonary problems – cannot tolerate metabolic rate 

 Physiologic

• Cardiovascular 

  • increased heart rate 

    • increased cardiac output 

• Pulmonary 

  • increased oxygen consumption 

  • increased respiratory rate 

• Metabolic 

  • decreased production of albumin 

  • increased production of acute phase proteins 

  • altered drug metabolism 

• Immune System 

  • immune system function enhanced during fever 

hypothermia

• Mild hypothermia 32-35^oC (89.6-95^oF). 

• Moderate hypothermia 28-32oC (82.4-89.6^oF) 

• Severe 

• hypothermia < 28oC (<82.4^oF) 

Etiology 

• Long extractions from car accidents 

• Water 

• Outside sports 

• Populations at Risk 

  • Elderly

  • very young 

  • individuals with chronic diseases 

Manifestations 

• decreased heart rate 

• decreased cardiac output 

• development of coagulopathies 

• depressed CNS 

pain

whatever the patient says it is

REM

• 25% of sleep 

• Decrease in temperature 

• More psychologically restorative 

• Towards end of sleep cycle 

• Dreams  

• Decreased with alcohol if drinking before bed

Sleep Stages 1-4

• Stage 1 

  • light sleep

• Stage 2 

  • 50% of sleep 

• Stage 3 

  • 15% of sleep 

  • More physiologically restorative 

• Stage 4 

  • 15% of sleep 

  • deep sleep

circadian rhythm

• Cortisol peaks an hour before you wake up 

  • In depressed people cortisol stays up in the afternoon 

• Depressed people have prolonged sleep 

• Stomach most likely to be empty in the morning 

• Temperature goes down as you start to fall asleep but is highest in the evening

spinothalamic tract

• Transmitted from thalamus to sensory cortex 

• Fast Pain vs. Slow Pain 

• A delta axons - myelinated 

• C fibers - unmyelinated 

pain manifestations

• increased heart rate 

• increased blood pressure 

• increased respiratory rate 

• dilated pupils 

  • Stress response 

• pallor and perspiration 

• nausea and vomiting 

• urine retention 

• elevated blood glucose 

  • From stress response 

visceral pain

• visceral organs 

• Hard to locate exactly where pain 

  • Afferent pathways from the heart are shared with pathways in other areas - left arm, chest, jaw

  • all bladder pain refers to the right shoulder

• Brain cannot differentiate  

somatic pain

muscles, tendons

cutaneous pain

superficial structures

referred pain

pain that is perceived at a site different from its point of origin but innervated by the same spinal segment