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Answered: - Test 4 Blueprint / Content Summary (reminder: these blueprints


Good evening, I need the best way to study for my Pathophysiology exam, I have attached the blueprint.


Test 4 Blueprint / Content Summary

 

(reminder: these blueprints contain MOST of content

 

on a test,

 

but not necessarily 100%)

 

40 questions in same format as other tests.

 

Neurologic Disorders (10-14 questions)

 

1.

 


 

ophthalmologic disorders

 

general terms (be sure you understand mydriasis, miosis, nystagmus, papilledema)

 

o mydriasis?pupil dilation?sympathetic (adrenergic) response that occurs upon

 

exposure to darkness: a sympathetic branch of the cranial nerve that innervates the

 

muscles around the pupils releases norepinephrine attaches to adrenergic receptor

 

sites on those muscles & cause them to contract, which dilates the pupil.

 

o miosis?pupil constriction?parasympathetic (cholinergic) response that occurs upon

 

exposure to light: a parasympathetic branch of the cranial nerve that innervates the

 

muscles around the pupils releases acetylcholine attaches to cholinergic receptor

 

sites on those muscles & cause them to relax, which constricts the pupil.

 

disorders:

 

o cataracts: usually age-related, slow development of protein on the lenses so that

 

vision diminishes.

 

o glaucoma?narrowing of the angles of the eyes so that aqueous humor cannot be

 

properly absorbed intraocular pressure increases and impedes peripheral vision;

 

open-angle usually slow and painless, closed-angle more acute and painful from the

 

sudden pressure.

 

o AMD?age-related macular degeneration?the macula coordinates central vision, so

 

that is what is affected in this disease; often a dark spot is seen in the middle of the

 

central visual field.

 


 

2.

 


 

CNS disorders: general concepts:

 

concepts of ICP (intracranial pressure) vs CPP (cerebral perfusion pressure)?body keeps

 

these two in balance

 

o ICP very reliant on CPP & vice versa

 

o abnormal CPP often results in increased ICP:

 

CPP can be too low in states like hypotension, hypovolemia, atherosclerosis of

 

carotid arteries, etc?this can cause ischemia & hypoxemia of the

 

braincerebral edema increased ICP

 

or CPP can be too high (ex?high BP) and cause intracerebral bleeding, etc

 

edema increased ICP.

 

o increased ICP (IICP)

 

causes of increased ICP (IICP): often caused by cerebral edema secondary to:

 


 

CPP abnormalities ischemia & hypoxia;

 


 

irritants like hemorrhage, infection, acidosis

 

? almost any kind of brain problem has potential to generate cerebral

 

edema & therefore increased ICP.

 

body cannot tolerate much of an increase in ICP; if ICP is increased:

 

? prevents oxygenated blood from being able to easily get into brain

 

arteries (ie, decreased CPP)

 

? causes malfunction of various parts of brain, with varied sequela

 

general sequela / S&S of IICP

 

o change in level of consciousness (spectrum of changes, depending on degree of IICP)

 

o pressure on respiratory centers Cheyne Stokes (altered breathing pattern in

 

comatose state; pressure other parts brain stem decerebrate & decorticate

 

posturing (also only found in coma states)

 

1

 


 

certain reflexes can be affected, such as Babinski?s (plantar reflex)?in someone over

 

2 years old, positive Babinski?s usually indicates cerebral lesion of some sort (such as

 

edema, tumor, etc); also loss of primitive but essential reflexes like cough & gag &

 

swallowing.

 

o papilledema

 

o if IICP gets bad enough can cause brain herniation

 

specific sequela / S&S of IICP as categorized according to whether there is a diffuse problem

 

or a focal one in the brain

 

o diffuse problems usually associated with:

 

generalized S&S such confusion & other signs of decreased LOC (spectrum of

 

changes, depending on degree of IICP)

 

usually fairly symmetric changes in the body bilaterally, including reflex

 

changes.

 

o focal problems:

 


 

usually associated with asymmetric, unilateral findings-- focal S&S in the

 

body, depending on where in the brain the lesion is

 

if there is focal pressure (lesion, edema, etc) on motor tracts in brain there

 

would likely be paresis (and maybe reflex changes) on contralateral side of

 

the body below the neck (opposite to where the brain lesion is)

 

if there is focal pressure on CNs there would likely be dysfunctions of face,

 

eye movement, etc, on contralateral side

 

treatment for brain disorders: most interventions for brain-related problems are geared

 

towards lowering ICP by:

 

o keeping head of bed up at ~ 30 degrees

 

o keeping BP not too high & not too low

 

o sometimes giving diuretics.

 

o

 


 


 


 


 


 

3.

 


 

specific CNS disorders

 

vascular disorders: stroke (AKA cerebrovascular accident [CVA], AKA brain attack)

 

o causes: list on pg 7 of notes (generally same risk factors as CV disease & HTN)

 

o 2 types?ischemic & hemorrhagic

 

o ischemic?thrombotic, embolic [& TIA]

 

thrombotic-- thrombus forms in arteries going to brain or within brain itself &

 

causes ischemia to distal tissue

 

embolic?clot breaks off from a thrombus (ex?clots in left atrium that develop

 

in left atrium during atrial fibrillation can become emboli) & lodges elsewhere

 

in a cerebral artery & causes ischemia

 

TIA?transient ischemic attack?NOT a true stroke

 

o hemorrhagic?intracerebral bleeding from head injury, burst aneurysm, HTN, coagulation

 

disorders, etc

 

o

 


 

S&S of stroke depend on area of brain it happens?right or left hemisphere, cerebellum,

 

brain stem

 

hemispheric stroke: S&S usually manifest as some combination of the following:

 

o paresis on contralateral side below neck & shoulders because of decussation

 

of corticospinal tract (AKA pyramidal tract).

 

o paresis on contralateral side above neck & shoulders

 

o hemisphere-specific problems like aphasia & inability to do math (would mean

 

a lesion in left hemisphere) or decrease in spatial understanding, insight into

 

condition, & left-sided neglect (would mean a lesion in right hemisphere).

 

cerebellar stroke: vertigo, nystagmus, loss of balance

 

brain stem: depends on where?respiratory problems, CV problems, CN problems

 


 

o

 


 

tx: clot-busting drugs sometimes can be used in ischemic stroke, also anticoagulants

 

like heparin to prevent further clots; for hemorrhagic stroke usually need to treat cause

 

like performing surgery to fix aneurysm; also, for all types strokes-- any interventions

 

that help decrease hypoxia & IICP HOB up, give O2, BP management.

 

2

 


 


 


 

degenerative disease of brain

 

o Alzheimer?s?type of dementia caused by abnormal accumulation of amyloid in

 

brain tissue & the presence of neurofibrillary tangles inside cell bodies of neurons

 

of brain both situations interrupt nerve signals & cause S&S such as severe

 

memory, behavioral, and motor changes

 

o Parkinson?s?caused by decrease in dopamine in the basal ganglion of the brain,

 

which are part of the extrapyramidal system

 

without inhibitory effect of dopamine, acetylcholine is ?free? to bombard

 

receptor cells with excitatory impulses

 

this cholinergic over-activity causes a ?circuit-overload? effect on muscles

 

that is manifested as rigidity (ex??cog-wheel rigidity?), slow movement

 

(hypokinesia), tremors such as pill-rolling tremor (dyskinesia), shuffling

 

gait (AKA Parkinsonian gait, or basal ganglion gait).

 

treatment is to give dopamine and anticholinergic medication.

 

o multiple sclerosis

 

autoimmune disorder in which our own T-cells attack myelin sheaths of

 

random axons in the brain.

 

this eventually causes scarring & sclerosing of the myelin sheath cells,

 

affecting the parts of the body controlled by those areas; this is called

 

demyelination

 

since myelin sheaths are important in maintaining velocity of nerve

 

signals, damage to the myelin results in slowed or interrupted signals

 

S&S?asymmetric, varied areas, depending on damage sites; ex-weakness of an extremity, bladder problems, ataxia, vision problems.

 


 


 


 

other brain / meningeal disorders

 

o migraines

 

intense, often one-sided headache caused by hyperreactivity of

 

combination of vascular and neural responses, causing pain and other S&S

 

often has individual triggers and stages that include prodrome (which

 

sometimes involves an aura of some sort), actual pain, and postdrome

 

tx?trigger-avoidance, NSAIDS (to counter inflammatory prostaglandin

 

involvement), and abortive drugs which should be taken as early into the

 

migraine as possible to stop the evolvement of events.

 

o seizures?sudden, chaotic discharge of neurons in brain

 

called epilepsy if a chronic, usually congenital origin

 

2 categories of szres?general (pt always unconscious, tonic-clonic

 

movement) & partial (varied degrees of consciousness & motor

 

involvement, usually local)

 

post-seizure state of re-organization of brain signals called post-ictal state

 

?pt groggy, confused.

 

if seizure continues unabated it is called status epilepticus.

 

o meningitis (infection /inflammation of meninges)

 

inflammation causes increased permeability of meningeal structure

 

edema this irritates nerve endings of spinal meninges plus often causes

 

cerebral edema

 

S&S:

 

photophobia, headache, irritability, restlessness, confusion

 

neck stiffness; also, positive Brudzinski?s and Kernig?s signs?these

 

are maneuvers that ?stretch? the inflamed meninges & cause pain

 

and/or stiffness in bending neck & knees.

 

CSF?high protein (due to presence of bacteria & exudates from

 

inflammatory response), high WBCs, low glucose (bacteria feed on

 

glucose).

 

types of meningitis:

 

3

 


 


 


 


 

viral usually mild S&S?viral meningitis also called aseptic

 

meningitis

 

worse type of meningitis is meningococcal?virulent endotoxin that

 

can cause petechiae and purpura?skin involvement

 


 

4. peripheral nervous system disorders

 

neuromuscular junction disorders?myasthenia gravis

 

o caused by autoantibodies that destroy acetylcholine receptors at the distal end of

 

neuromuscular junction

 

o characterized by weakness that gets worse with activity and better with rest

 

o tx?cholinesterase is an enzyme that breaks down the extra acetylcholine in the

 

junctional synapse as part of normal ?clean up?, so by giving anti-cholinesterase

 

drug, less acetylcholine is broken down & more is available to compensate for less

 

receptors

 

o because T-cells are involved, sometimes thymectomy helps (T-cells mature in

 

thymus)

 


 

Endocrine Disorders (10-14 questions)

 

1.

 


 

2.

 


 

thyroid problems

 

hyperthyroidism?a state of excess T3 & T4 secreted by the thyroid.

 

o most common cause is autoimmune disease called Graves? disease, in which

 

autoantibodies mimic TSH by fitting into TSH receptors on the thyroid & causing it to

 

over-secrete T3 & T4

 

o manifests as state of metabolism overdrive?pt is often nervous, irritable, can even

 

have psychosis & hallucinations; CV ? tachycardia; GI?increased appetite but pt

 

stays very thin & fatigued from hypermetabolism; exophthalmus?tissue build-up

 

behind eyes; sweating, warm skin; higher body temp.

 

o goiter from increased activity of thyroid cells hyperplasia & hypertrophy

 

o lab?T4 high, TSH low due to negative feedback

 

o extreme version ? thyroid storm (AKA thyrotoxicosis)?extreme tachycardia, HF,

 

shock, temp of 103-105, agitation, delirium, seizures

 

o tx?anti-thyroid meds and/or thyroidectomy

 

hypothyroidism--low thyroid hormone secretion

 

o one of most common causes is Hashimoto?s thyroiditis?autoimmune disease in

 

which autoantibodies directly destroy tissue scarring, nonfunctional tissue

 

o another cause, uncommon these days because we add iodide to our salt?endemic

 

iodide deficiency (since iodide is a key ingredient in molecular structure of T3 & T4);

 

if mother is iodine-deficient, her fetus won?t develop properly child is born with

 

stunted mental & physical growth called cretinism

 

o S&S?opposite of hyperthyroidism; also, face takes on a bloated appearance called

 

myxedema

 

o lab?T4 low, TSH high

 

o extreme version of hypothyroidism?myxedema crisis, or coma?when

 

hypothyroidism leads to unconsciousness, hypotension, hypoventilation.

 

o goiter from thyroid tissue trying to compensate for undersecretion

 

problemshyperplasia & hypertrophy

 

o tx for hypothyroidism?synthetic thyroid medication

 

if hyperthyroidism caused by pituitary hypersecretion of TSH TSH & T4 both high; if

 

hypothyroidism caused by pituitary hyposecretion of TSH (ie, a pituitary problem, not a

 

thyroid one)

 

calcium movement:

 

4

 


 

o

 

o

 


 

PTH (parathyroid hormone) largely responsible for calcium movement; calcitonin from

 

thyroid is second influence; they counterbalance each other.

 

PTH secreted when there is need for calcium to be used in other parts of body, or when

 

there is a state of hypocalcemia, because PTH increases movement of Ca from bone to blood

 

(resorption) by stimulating increase in osteoclastic activity

 

any situation that pathologically increases PTH results in hypercalcemia increase

 

chance for kidney stones, also hyperpolarization of RMP of muscle cells, so weakness,

 

lethargy; also, less calcium in bone, so osteoporosis

 

any situation that pathologically decreases PTH results in hypocalcemia?all the

 

opposite problems, including tetany, muscle spasms, positive Chvostek?s (from

 

hypopolarization of RMP?remember that hypocalcemia causes increase in

 

permeability of cells to Na+ more Na+ in cell = increased positivity =

 

hypopolarization).

 

calcitonin does all the opposite (ie?calcium goes into bone, etc).

 

osteoporosis

 

o variety of causes:

 

long-term hypocalcemia problems (like in CRF)

 

nephrotic syndrome

 

PTH increase

 

calcitonin decrease

 

age-related change in which the balance of osteocyte vs osteoclast is tipped

 

toward too much osteoclastic activity calcium resorption increases & bone is

 

left weakened

 

menopausal changes: significantly less estrogen (atrophied ovaries) ultimately

 

means less stimulation of bone-building by osteocytes and more activity by

 

osteoclasts, so more bone resorption.

 

o spectrum of amount of weakening includes osteopenia?loss of bone, but not as bad

 

as osteoporosis.

 

o tx?drugs that decrease osteoclastic activity and/or or build up calcium, like calcium

 

supplements

 


 


 

o

 


 

resorption means bringing something

 

back into blood; most often refers to

 

calcium coming into blood from bone?.

 

sometimes called ?bone resorption.?

 


 

3.

 


 

adrenal disorders

 

a.

 

Cushing?s syndrome or disease?a state of hypercortisolism &

 

hyperaldosteronism

 

1)

 

caused by:

 

exogenous steroids, or

 

an endogenous problem such as excess ACTH from pituitary

 

tumor

 

2)

 

sequelae of hypercortisolism

 

increased glycogenolysis & gluconeogenesis (these are

 

metabolic activities that cortisol increases normally, but with

 

Cushing?s are pathologically increased

 

hyperglycemiaglucosuria & polyuria & insulin resistance

 

ie, S&S of Type II diabetes

 

abnormal breakdown of adipose tissue (lipolysis) truncal

 

obesity, moon face, ?buffalo hump??ie, ?cushinoid appearance;?

 

also, increased LDLs & risk for atherosclerosis; general

 

weight gain

 

5

 


 

abnormally catabolized protein:

 

muscle weakness & wasting, especially in arms &

 

legs

 

skin fragility

 

bone cell breakdown hypercalcemia, hypercalcinuria higher

 

risk of kidney stones, osteoporosis, pathological fractures.

 

weakened collagen fibers skin fragility bruising,

 

striae

 

interruption of arachidonic pathway so that the protective,

 

positive effects of prostaglandins are inhibited:

 

stomach lining more at risk for peptic ulcers (usually

 

stomach lining protected by prostaglandins)

 

easier bleeding (from blocking of thromboxane, a

 

clotting product that has prostaglandin as precursor)

 

peripheral vasoconstriction (prostaglandins act as

 

vasodilators, so when suppressed, vasoconstriction

 

results) HTN

 

immunocyte function easier to get infections

 

sequelae of hyperaldosteronism:

 

increased water retention

 

hypokalemia

 

other: if there is also hypersecretion of androgens, sometimes

 

hirsutism is present

 

dx?draw cortisol levels at different times of the day

 

tx?withdraw or decrease exogenous steroids; fix pituitary or

 

if

 

that is the problem; give drugs that block aldosterone if

 


 


 

3)

 


 

4)

 


 

5)

 

6)

 

adrenal tumor

 

necessary.

 

b.

 

Addison?s disease (hypoadrenalism)?a state of hypocortisolism &

 

hypoaldosteronism

 

1)

 

cause: most frequent one is autoimmune attack on adrenal gland

 

with

 

resultant destruction of tissue; other possible causes includes

 

pituitary

 

problem (hypopituitarism).

 

2)

 

sequelae of hypocortisolism: hypoglycemia, which results in

 

fatigue,

 

weakness, apathy, confusion; also anorexia, N, V, D,

 

weight loss

 

3)

 

sequelae of hypoaldosteronism: increased excretion of Na and H20

 

by distal

 

tubule into urine low blood volume, dehydration; if bad

 

enough, can have

 

severe hypotension, called Addisonian crisis.

 

4)

 

tx?steroids, aldosterone, high-salt diet (within reason!)

 

4.

 


 

DM--diabetes mellitus (disorder of endocrine pancreas)

 

a.

 

DM is characterized by:

 

1)

 

hyperglycemia & glucosuria, and also (most of the time) long-term

 

problems

 

that are system-wide

 

2)

 

usually also polyuria & polydipsia, so DM is a DRY disease.

 

3)

 

3rd ?P? is polyphagia, excess hunger, seen in DM Type I.

 

b.

 

diagnosis / monitoring

 

1)

 

FBS (fasting blood sugar) > 126 on two occasions (norm = 70 to 99)

 

6

 


 

2)

 


 

Hgb A1C: the percentage of glucose-carrying Hgb molecules over

 

the

 

lifespan of an RBC; norm around 4%; aim for diabetics?keep

 

it < 7%; high

 

A1C = high average daily blood glucose

 

c.

 

Type I DM

 

1)

 

cause: autoantibodies destroy pancreatic tissue NO INSULIN

 

2)

 

2 categories of acute sequelae of no insulin:

 

hyperglycemia & its untoward effects, including dehydration.

 

no cellular energy source

 

3)

 

hyperglycemia & its untoward effects

 

BS?s (blood sugars) of untreated type I diabetic usually run

 

200 to 300

 

high BS exceeds renal threshold & glucose ?spills? into

 

urine high urine osmolality H2O drawn into urine from

 

tubular cells polyuria & dehydration polydipsia, dry skin,

 

dry mucus membranes, etc.

 

4)

 

no cellular energy source

 

after all glycogen is used up, gluconeogenesis begins fat

 

breaks down first, then muscles (protein) ketonemia &

 

ketonuria acidosis

 

patient stays thin & nutritionally deprived despite polyphagia.

 

if not treated, side effects of gluconeogenesis can lead to DKA

 

(diabetic ketoacidosis); S&S:

 

o ABGs show metabolic acidosis

 

o patient might have acetone breath (ketones are being

 

blown off)

 

o might have Kussmaul respirations to blow off CO2 &

 

bring up pH.

 

extreme state patient could become unconscious (from

 

irritating effects of acidosis on brain tissue)?this would be a

 

form of diabetic coma.

 

5)

 

tx?insulin

 

d.

 


 

Type II DM

 

1)

 

patho begins with increased fat cells in the body, which causes wide

 

spread

 

resistance to insulin

 

SOME glucose is getting into the cells from the blood, but

 

some is NOT, so the glucose in the blood increases

 

pancreas reacts to this continued hyperglycemia by increasing

 

secretion of insulin hyperinsulinemia

 

no matter how much insulin gets secreted, still can only get a

 

small portion of glucose into cells due to their insulin

 

resistance eventually pancreas ?poops out?? beta cells ?run

 

out of steam? & there is decreased insulin production

 

continued hyperglycemia

 

2)

 

S&S- hyperglycemia & glucosuria, like type I, but no DKA or weight

 

loss because there is still SOME glucose getting into cells.

 

since this is slow process, sometimes S&S very subtle?mild

 

polydipsia & polyuria, fatigue

 

7

 


 

also, BS?s can get very high ? 400-900?without patient

 

realizing it; this can cause extremely high serum osmolality,

 

polyuria, & dehydration; this acute combination known as

 

HHNK?hyperglycemic, hyperosmolar, nonketotic state

 

extreme state patient can become unconscious (usually

 

from brain cell dehydration)?this would be another form of

 

diabetic coma.

 

3)

 

tx?diet, weight loss, various combinations of meds, including

 

sometimes

 

insulin

 


 


 

f.

 


 

long-term problems associated with both types DM

 

1)

 

angiopathy, from toxic effects of glucose molecules on lining of

 

arterial

 

vessels

 

microangiopathy?damage to small vessels

 

o diabetic retinopathyblurred vision, blindness

 

o kidney arteriolerenal failure

 

o capillaries of skin easy bruising

 

macroangiopathy?damage to medium & large vessels?

 

stroke, CAD, aneurysms, PAD.

 

2)

 

neuropathy due to angiopathic ischemia to nerves in various tissue

 

(plus

 

direct toxicity of glucose)

 

o peripheral neuropathy?burning, pain, numbness of legs & feet

 

that can lead to high risk of trauma

 

o autonomic neuropathy?autonomic nervous system affected-gastroparesis, bladder control problems, ?silent MI.?

 

3)

 

phagocytic damage from glucose toxicity high risk of infections

 

(UTIs, yeast

 

infections, non-healing sores)

 

g.

 

metabolic syndrome?a cluster of conditions that greatly increases a

 

person?s risk for

 

heart disease?type II DM, elevated LDLs & decreased HDL,

 

HTN, abdominal

 

obesity.

 

e.

 


 

hypoglycemia (BS <70)

 

1)

 

etiology-- decreased food intake & other nutritional factors; in case

 

of

 

diabetes, can occur from too much anti-diabetic medication

 

such as insulin

 

2)

 

S&S?fatigue, shakiness, irritability, sweating?

 

occur from effect of counterregulatory hormones.

 

3)

 

tx?orange juice / sugar; IV dextrose; glucagon.

 

4)

 

extreme state hypoglycemic coma (called insulin shock or

 

insulin coma

 

if due to too much insulin); much more dangerous state

 

than diabetic

 

extreme state.

 

GI Disorders (10-14 questions)

 

Disorders of stomach & intestines

 

1.

 


 

problems of esophagus & stomach

 

a.

 

gastritis?inflammation of stomach lining

 

1)

 

acute?usually due to ETOH, NSAIDS; heals when cause is taken

 


 

away

 

8

 


 

2)

 

is

 

factor

 

b.

 


 

c.

 


 

chronic?may be autoimmune etiology; important possible sequela

 

development of pernicious anemia due to decrease in intrinsic

 

production.

 

GERD?reflux disease

 

1)

 

S&S-- heartburn, sometimes coughing

 

2)

 

if chronic & severe enough, can develop dysplasia of esophagus?

 

precancerous condition called Barrett?s esophagus.

 

hiatal hernia?protrusion of part of stomach into thorax

 


 

2.

 


 

PUD?peptic ulcer dz

 

a.

 

chronic inflammation of stomach and/or duodenum resulting in

 

breakdown of

 

luminal lining & ulcerations

 

b.

 

causes?NSAIDs (inhibit prostaglandin), ETOH, smoking, chronic dz,

 

genetics

 

1)

 

most common triggering cause?Helicobacter pylori (H. pylori)

 

2)

 

bacteria ingested via oral/fecal route burrows through mucous

 

layers &

 

attaches to epithelium (one of few bacteria to thrive in

 

HCl) colonizes,

 

creates favorable ulcer environment

 

c.

 

S&S

 

1)

 

painless; OR can have pain after meals

 

2)

 

hematemesis (coffee ground or bloody); melena from digesting

 

blood

 

3)

 

anemia

 

4)

 

perforation possible

 

d.

 

tx?antacids, H2 blockers, PPI?s, antibx

 

3.

 


 

IBD?inflammatory bowel dz-- chronic inflammation of walls of intestines

 

a.

 

different from irritable bowel syndrome (IBS), which is not an

 

inflammatory dz

 

b.

 

2 types?Crohn?s, ulcerative colitis

 

c.

 

Crohn?s

 

1)

 

most of time ileum & cecum involved?transmural, patchy areas

 

inflammation

 

2)

 

autoimmune dz, so other sites of body may have S&S of

 

inflammation?eyes

 

(iritis), arthritis, vasculitis.

 

3)

 

S&S?pattern of remissions & exacerbations of pain, bloody diarrhea

 

(hematochezia), malnutrition

 

4)

 

possible sequelae: intestinal obstruction, fistulas, perforation

 

d.

 

of colon

 

colon is

 


 

ulcerative colitis

 

1)

 

rectal & sigmoid colon are most common places, but can involve all

 

-- not small intestines

 

2)

 

inflamed areas are confluent but not transmural

 

3)

 

S&S much like Crohn's but more inclined to get dehydrated since

 

where water usually absorbed.

 


 

4.

 


 

intestinal obstruction

 

a.

 

can be partial or complete occur anywhere in intestines

 

b.

 

types

 

1)

 

direct blockage?tumor, hernia

 

2)

 

slowed / absent peristalsis?paralytic ileus (sometimes happens

 

post

 

surgery?prevent by early mobility)

 

9

 


 

3)

 

ischemic / strangulation type situation: intussusception?

 

telescoping of one

 

portion of bowel into another; volvulus?twisting

 

of intestine

 

c.

 

S&S?pain, distention, N, V, dehydration, lyte imbalance; tx?prevention

 

by keeping

 

pt as mobile as possible, NG tube to relieve distention, fluid & lyte

 

replacement,

 

surgery.

 

5.

 


 

diverticular disease

 

a.

 

diverticulosis?state of having diverticulum (outpouchings of muscle layer

 

of lower

 

intestines into lumen); most of time asymptomatic

 

b.

 

diverticulitis?diverticula become inflamed, infected; LLQ pain, fever,

 

leukocytosis

 

6.

 


 

appendicitis /peritonitis

 

a.

 

inflammation of appendix; S&S ? periumbilical pain, RLQ pain, N, V,

 

anorexia.

 

b.

 

peritonitis?inflammation of peritoneum of abdomen

 

1)

 

can occur with appendicitis or any other situation in which local in

 

which local

 

inflammation spreads or gut contents are spilled into

 

abdomen.

 

2)

 

S&S?pain upon movement, rebound tenderness.

 

Disorders of accessory organs

 

1.

 

jaundice (icterus)--deposition of excess bilirubin under skin, mucous

 

membranes, sclera of eyes; types (based on the part of the bilirubin cycle that has

 

been altered)?prehepatic,

 

hepatic, posthepatic

 

a.

 


 

prehepatic? too much unconjugated bilirubin in blood

 

1)

 

this means lab results would show high indirect bilirubin & normal

 

direct

 

bilirubin

 

2)

 

basic etiology = hemolytic problems

 

o RBCs are being broken down at greater than normal rate or

 

amount greater amount of unconjugated bilirubin in blood

 

because liver can only normally conjugate a certain amount

 

high...

 


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