STUDY-FOCUS-EXAM AH II EXAM 2022/2023 LATEST UPDATES, Exams of Nursing

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AH II Exam 3 Topic list

The number/s in parentheses indicate and approximation of weight/ number of

items for each topic

Week 6 (Apply these selected disorders/diseases to the Medical Surgical

Mantra)

GI- motrin (always w/ food) &

remember that liver pts have issues coagulating, because they are missing the intrinsic factors

Pancreatitis (4-5): alcohol/drug consumption and fatty diet, chronic does not require

hospitalization PATHO: digestive enzymes are trapped in the pancreas, so it is autodigesting itself

(food will cause pain)-makes it susceptible to infection & sepsis= they are prone to SIRS= death by

MODS & hypovolemic shock; because of capillary leakage= fluid in their lungs

TX: NG tube (decompress the stomach contents-enzymes that were eating away at the stomach,

which will decrease pain), repositioning, deep cough, insentive spirometer (IS)-all of the respiratory

stuff is to keep the fluids moving , Protonix, IV fluids, narcotics, TPN (for chronic or last for an

extended period of time)=PICC line, & antibiotics-prophylaxis; NPO so the pancreas can heal and acids

are not secreted, diet is per toleration, beginning w/ clear liquid, and IV lipase & amylase

SxS: upper abd pain, pain radiating to back, n/v, fever, abd tenderness

LABS: lipase & amylase

STUDY-FOCUS-EXAM AH II EXAM

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STUDY-FOCUS-EXAM AH II EXAM

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Upper GI bleed (1-2): gastritis, peptic ulcer disease, varices from cirrhosis, anything

that causes bleeding-leads to hypovolemic shock- you will worry about bowel perforation=sepsis from peritonitis hemodynamic stability-tachy & HTNsive- draw a type and screen (T&S), give bolus, start blood transfusion, pt does not have clotting factors

• Increased incidence in older adults, women, and anyone who chronically uses NSAIDs
• Sudden (most serious) or slow onset; severity based on where the bleeding begins: venous, capillary or arterial (arterial bleeding is profuse- bright red, because it has not come into contact w/ stomach acid) - Types of bleeding : obvious = hematemesis (fresh & bright or “coffee grounds- when the blood sits in the stomach and the acid changes it”, melena- black, tarry stools (color caused by digesting blood & iron ) & occult= small amounts that appear in gastric secretions, emesis, or stools; can only be detected by guaiac test - The longer the blood is in the intestines the darker the stool, as Hgb breaksdown and releases iron - CAUSES: esophageal, stomach/duodenum , drug-induced, or systemic diseases
  1. Esophageal origins- chronic esophagitis: GERD, mucosa-irritating drugs, alcohol, & smoking; Mallory-Weiss tear; esophageal varices
  2. Stomach/duodenal origins- gastric cancer (steady blood w/ growth and ulceration), hemorrhagic gastritis, PUD (50% of UGIs that bleed, related H.pylori or NSAID use- especially in the gero pop), polyps, & stress-related mucosal disease (stress ulcers, severe burns, trauma, or major surgery; causes greater erosion than PUD)
• ASSESS/MNG: 80%-85% of pts w/ massive bleeds will spontaneously stop- cause still identified and TX initiated; check BP, RR, HR, cap refill, pallor, & JVD; check LOC & VS every 15-30 mins, shock SxS (low BP, rapid/weak pulse, increased thirst, cold, clammy skin, restlessness, etc.); focused abd assessment (bowel sounds, the feel of the abd-tense/rigid= perforation/peritonitis, distention or guarding); HX: must include- previous bleeding, recent weight loss, and if they have had a blood transfusion before
• LABS: CBC, BUN, electrolytes, CBG, liver enzymes, ABGs, type & cross, & PT; specimen orders for emesis, stools and urine
• RN INTERVENTIONS: Fluid replacement (usually LR 1st, but phys. & lab findings will dictate), have 2 IVs w/ one at least 16-18 g (for blood transfusion), blood admin (whole, PRBCs, FFP; PRBCs are preferred to prevent hypervolemia & immune reactions)- H&H checked often; O₂, foley , & central line
• DIAGNOSTICS: endoscopy-primary tool used (may require lavage, or aspiration of stomach contents w/ large-bore tube (Ewald tube) to remove clots), angiography- used if an endoscopy cannot be done, very invasive procedure: a catheter is placed into the left gastric or superior mesenteric artery until bleed is found; diagnoses= hypovolemia, ineffective tissue perfusion, anxiety, ineffective coping, risk for aspiration, or decreased cardiac output
• Other care: Endoscopic hemostasis therapy- coagulates or thromboses a bleeding artery; used for

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gastristis, Mallory-Weiss tear, esophageal/gastric varices, bleeding PUs, & polyps; thermal probe - applies heat to the site (one of the most common), electrocoagulation probe - the multipolar ones are the other most common used, argon plasma coagulation- delivers a current w/o contact (APC), neodymium yttrium-aluminum-garnet laser (Nd-YAG), surgery- only if bleeding continues, 2000 mL have been rapidly transfused, or pt in shock for over 24 hrs: high rate of mortality for gero pop; drug therapy: decreases blood & HCl acid & neutralizes HCl acid- epi= hemostasis during endoscopy (ulceration)=edema which places pressure on bleeding area, acid reducers=alter platelet function/clot stabilization, histamines (H₂-blockers)= inhibit histamine action & decrease HCl secretion (cimetidine- Tagamet, ranitidine- Zantac), PPIs= suppress secretions (H⁺, K⁺, & ATPase)/gastric acid pump (pantoprazole-Protonix , esomeprazole- Nexium)-part of standards, but not proven to control active bleeding-must be admined. w/ NSAID or H₂ blocker; somatostatin analog octreotide (Sandostatin)-reduces blood flow/acid secretion (is an IV bolus-given up to 6 dys after bleeding stops)

• CAUTIONS/CONTRAS: sedatives= caution, contra.= anticholinergics
• EDUCATION: pts w/ hx of chronic gastritis, cirrhosis, or PUD, has had a bleed before at high risk, avoid irritants- alcohol, smoking, & stress, only take prescribed meds, how to check for blood in emesis or stools, adverse effects of bleeding, if using aspirin use coated tablets, pts w/ esophageal varices must have upper resp. infections treated immediately
• Pallor, diaphoretic, distended bowels, VS, slow cap. refill, feels “lightheaded”, vomitus, leave stool and urine for you to see
• Bolus 0.9% & PRBCs
• PPIs, coughing/deep breathing, NG tube, ambulate, & narcotics - Can cause peritonitis and bacterial infection (gram negative),

causing Sepsis

- Shock (lack of perfusion to tissues): BP is tanking= pressors, large

gauge IV-must be 20g or higher 16g is best, bolus, blood-be careful

w/bolus and blood together can cause hypervolemia, O₂

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Chronic alcoholism labs: thyamine, elevated liver enzymes (digestive

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enzymes), elevated bilirubin, low H&H and albumin

Dumping syndrome !-2): shortened gut, bariatric surgery, Whipple; insulin is leaked

too quickly (hypertonic)---leads to hyperglycemia and hypotension, you feel lightheaded, n/v, feel like you are dying Empties the stomach contents into the top part of the stomach too fast SxS: diaphoretic, tachycardic, anxious (hypotension)

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Pay attention to certain foods that are called slippery foods

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Mallory-Weiss tear (1): esophageal bleeding

• When a tear occurs in the mucosa at the esophagogastric

junction, medulla oblongata activates the vomiting

reflex

• Symptom= severe retching/vomiting

• Most pts will be self-healing, but not liver pts

• TX: endoscopic hemostasis therapy-if someone continues

to bleed; may need to be repaired (cauterized)

• Tear caused by retching

• Cirrhosis (5-6): what you will see- esophageal varices= portal hypotension (TX: beta

blockers)- the vessels become high pressurized, which makes them become like vericose veins= weakened-pop-and bleed into their stomach-no intervention =death quickly ; findings for endstage pts= ascites-hypoalbuminemia, jaundice, bleeding esophageal varices-secondary to portal hypotension, hepatic encephalopathy-ammonia, LOC=alcohol withdrawal (seizures) or hepatic encephalopathy; they will look shocky

• Ascites= hyporalbuminemia - portal HTN= hydrostatic ?= low BP -if you’re not watching then

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you are chasing them away from the cliff, instead of just keeping them away= albumin , hepatic

encephalopathy (nitrogenous by product= ammonia & urea)-they can

present at anytime , can go into alcohol withdrawal-starts low grade, then can move to alcohol

seizures-give Ativan or other benzos; weigh them often

• LABS: CBC, ESR & CPR-indicates inflammation, albumin serum levels (will help us know if they have edema, along with BP-it will be low), AST, ALT, & proteins LFTs (liver

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function tests); may also find B vitamins are off, H&H-elevated white count, increased bilirubin (by product of the breakdown of red blood cells) and ammonia

- TX: albumin (hypoalbuminemia), blood (bleed), lactulose-binds to the ammonia levels (for hep. Enceph.)-LOC will decrease; diuretics (give w/ care- to prevent ascites, edema, and dropping their BP- spironolactone, beta blockers (if they have stable BP-will be diuresed to take away extra fluid)-is to treat portal HTN= no bleeding esophageal varices - We will be treating esophageal varices, bleeding, hepatic encephalopathy, alcohol withdrawal, edema **- Good liver means they will get urea, but w/o there is a build-up of ammonia

• Part of hep. Enceph. =axtrixsis=hepatic flop when you have a pt put out their** **flexed hands
• Fetor hepaticus=breath of death
• Your keeping them alive during your shift; there is no cure at this point**
• Watch for these pathologies, they come together often; along with acute alcohol withdrawal - Watch for signs of shock related to bleeding esophageal varices(LOC, diaphoresis), jaundice (elevated bilirubin-by product of the breakdown of Hgb/ for dark skin look at the sclera (hard palatte) for the yellowing, and often finger/toe nails, and palms **of hand/feet), and ….
• DIET: low protein & NA⁺; some places say high protein (can make it worse-** creating more ammonia), but will use low protein; same for renal and heart as well

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STUDY-FOCUS-EXAM AH II EXAM

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NASH: nonalcoholic steatohepatitis: inflammation and damage from a

STUDY-FOCUS-EXAM AH II EXAM

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build-up of fat in the liver (fatty liver); NOT CAUSED

BY ALCOHOL

You will still need to ask them if they drink alcohol often

Esophageal varices (1-2): usually occurs 2

nd

to cirrohosis of the liver;

which causes pressure in the hepatic portal= portal hypertension will

cause the esophageal varices to pop and bleed

• Branches of the vena cava & azygos vein w/ smaller

lower vessels

• TX: endoscopic hemostasis therapy, vasopression (ADH) &

octeotide (helps stop bleeding, especially in the splenic area)

(they vasoconstrict the vessels, slowing the bleeding down, but

not fixing, ice/cold water lavage-varices are visible for repair;

TIPS to repair; 09% bolus, blood admin (Hct),

• SxS: low BP, urine output decreases

• Endoscopic hemostasis therapy- coagulates or thromboses a bleeding artery; used for gastristis,

Mallory-Weiss tear, esophageal/gastric varices, bleeding PUs, & polyps; thermal probe -applies heat to the site (one of the most common), electrocoagulation probe - the multipolar ones are the other most common used, argon plasma coagulation- delivers a current w/o contact (APC), neodymium yttrium- aluminum-garnet laser (Nd-YAG), surgery- only if bleeding continues, 2000 mL have been rapidly transfused, or pt in shock for over 24 hrs: high rate of mortality for gero pop

Hepatic encephalopathy (1-2): build up of ammonia that leads to

decreased LOC ; TX: lactulose

**- Good liver means they will get urea, but w/o there is a build up of ammonia

• Part of hep. Enceph. =asterixis=hepatic flop when you have a pt put out their** **flexed hands
• Fetor hepaticus= breath of death
• Intervention= glasglow coma scale**

Fatty liver (1): pancreatits and cirrhosis

• CAUSES: DM, diet, alcohol/drug abuse, genetics, obesity….

• Once it happens it is hard to reverse

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Gastritis (1-2): inflammation of gastric mucosa=a breakdown in

the gastric mucosal barrier, leaving the stomach unprotected from

HCl acid and pepsin, one of the most common stomach problems

TX: endoscopic hemostasis therapy, stop eating the spicy foods, alcohol,

NSAIDS, etc., …..?

Disrupts capillary walls, that can lead to hemorrhage

RISKS: drugs (NSAIDS, aspirin, corticosteroids -irritate), diet (alcohol, spicy

food), H. pylori, stress

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Cause of B12 defiency-no intrinsic factor= diminished RBC production= pernicious/megaloblastic

(MCV= size of the blood cells) anemia

PATHO: wear down of mucosa layer= not intrinsic factor= parietal cells get damaged, because the

mucosal layer is not there to protect them from the secreted stomach acid

Bowel perf/peritonitis/SIRS (1-2): something ends creating a hole in

the gut, causing leakage of gastric bacteria (e coli, h pylori, etc.) and

HCl—can cause peritonitis, which will lead to SIRS (w/or w/o

infection)---leads to MODS

Cullen’s sign: bruising around the umbilicus, 2

nd

ary to

hepatitis Patho:

TX:

(Do not apply the mantra to these. You need to need know what these are

and why we do these diagnostics) Be prepared to answer these questions in

class

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TIPS (transjugular intrahepatic portosystmic shunt) procedure

(1): A TIPS procedure involves creating a pathway through the liver

that connects the portal vein (the vein that carries blood from the

digestive organs to the liver) to a hepatic vein (one of three veins that

carry blood from the liver to the heart).

• PCs: acute liver failure, hepatic encephalopathy,

hemorrhage, biliary injury, injury to surrounding

organs

(damage to blood vessels, fever infection,

bruising, bleeding TIPS thrombosis, TIPS

dysfunction, TIPS migration

• Lowers pressure on esophageal varices, so they do

not pop and bleed

• They can occupy the esophagus and into the top part

of the stomach

• Sengstaken Blakemore tub-goes down and has a

balloon that will provide pressure on the bleed

Vasopressors and octeotide or beta blockers to lower the pressure, prior to

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procedure

Bleeding: pallor, anxious, fidgety, diaphoretic, tachycardic, urinary

ouput decreases, increased lactic acid

Ice/cold water lavagae to stop bleeding and decompress their stomach

w/ an NG tube, but this can irritate the varices

Ice and/or heat therapies or cauterization can be used

NEURO: ALWAYS WATCH FOR

INCREASED ICP

OTHER INFO:

• Brain tumors= location- orginate w/in CNS, secondary tumors

from metastasis in other parts of the body; classification;

types

• Management: radiation, chemo therapies, analgesics,

anti- inflammatory (IVP), phenytoin, ranitidine

hydrochloride, stereotactic surgery (take out the tumor)

• Abscesses: purulent infection in the brain, can present like a

stroke or other neurologic issue (depends on what it is

pressing

against), diagnosed w/ CT, tx: antibiotics, aspiration

Week 7 (Apply these selected disorders/diseases to the Medical Surgical

Mantra)

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Frontal lobe= sexual, easily angered, judgement effected

safety measures: bed low, bed alarm, sitter/family, sit close to RN station

CVA (6-7): 2 types ischemic/thrombolic/embolic (3-4.5 hrs) &

hemorrhagic=HTN (no anticoagulant before the CT-non

contrasted)- need to get good perfusion to the brain, but not by

HTNive meds, so if you see it still on their order, call physician

to

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d/c- we need perfusion

SxS: unilateral facial droop or paralysis, slurred speech, neurologic changes,

drooling

Questions: Are you on any blood thinners? When was the onset? Do you have

a headache (subarachnoid or blood on the brain)-can be a key factor of a

hemorrhagic stroke?

TX (ischemic): IVP TPA (Tissue Plasminogen Activator= breaks up the clot

(clotbuster , 3-4.5hrs only-may be given a little later for someone young and

healthy, but may cause a bleed out ), anticoagulants (heparin/Coumadin);

antiplatelets, mercy? Surgery, lorazepam (antiepileptics), calcium channel

blockers, stool softeners, antianxiety meds

TX (hemorrhagic): craniotomy/burr holes/window, drain, etc.;

anticoagulants, antiplatelets; DO NOT GIVE ANY MEDS UNTIL THEY

HAVE SEEN THE NEUROLOGIST

LABS: rainbow, CBC, chemistries-liver, pancreas, kidneys, etc.), and coags

DIAGNOSTIC: non contrasted CT

CONCERNS: falls and aspiration

OT and SLP evaluation

Watch for SxS of: ICP, aspiration….....?

Contra-intuitive: do not give HTNsive meds, so you do not further drop their BP

TIAs are warning signs of a stroke

ASSESSMENT: cognitive, motor, and sensory changes, ??

COMPLICATIONS: hydrocephalus-causes the stroke,

vasospasms, rebleeding/rerupture

INTERVENTIONS: monitor ICP, safety (unilateral neglect), emotional support,

and education

MANAGEMENT: thrombolytic therapy, neuroprotective drugs, surgery=

carotid artery angioplasty w/ stenting, endarterectomy, extracranial-intracranial

bypass (surgeries can cause a clot to move),

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TBI (1-2) traumatic brain injury: sudden injury from trauma

(bump, jolt/kick, penetration)

Open/closed head injuries, fx

Coup or contrecoup injury= coup=one way (forward) & contracoup=

the opposite direction

Epidual hematoma/subepidermal hematoma= tearing bridging

Subdural hematoma=

COMPLICATIONS: hydrocephalus, brain herniation=travels down

the spinal colum, stroke in brain stem

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PRIORITY INTERVENTIONS: assessment, surgical intervent.,

postsurgical care=safety, priority nursing care in ED, d/c teaching

Frontal lobe= sexual, easily angered, judgement effected

safety measures: bed low, bed alarm, have bed rails up, sitter/family, sit

close to RN station-so they don’t hurt themselves or someone else

you see personality changes

Do not put them in restraints

Mentation changes

DO NOT GIVE ANY MEDS UNTIL THE NEUROLOGISTS SEES

THEM.

Bell's Palsy (1): mostly in the face, but rule out a focal stroke

SxS: visual disturbances, unilateral facial droop (usually, but can occur

to both sides), difficulty swallowing, hepatic lesion near their ear

TX: anti-inflammatories

It is the inflammation of vagal nerve #7 facial nerve

MG (1): myasthenia gravis

FINDINGS: resp. failure, slurred speech, ptosis (droopy eye),

difficulty swallowing, & dysphagia can lead to aspiration

pneumonia (PNA)

Breakdown of communication between muscles & nerves

TX: pyridostigmine- helps electrical signals travel between the nerves and

muscles, can reduce muscle weakness, must be taken several times a day,

because the effects don’t last long

Autonomic dysreflexia (1-2): sudden onset of HTN (severe) &

bradycardia, caused by a full bladder in a spinal cord injury

TASKS: HTT, VS, meds, digital stimulation (have them on their

left- side)=stimulates peristalsis & allows for impaction removal,

and straight caths throughout the day (can’t evacuate bladder)

Sit them up in bed for a bit, notify physician, palpate bladder,

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then straight cath—if it doesn’t work meds will be ordered

Empty bowels and urine at the start of the day, head to toe, VS, then

meds

You will need to palpate their bladder often

Give them lots of antispasmotics, often

(Valium)

Repsirations should still be normal

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TX: reposition so they are sitting up-can lower the pressure and

increase the pulse, assess bladder & bowels-dig. Stimulation and red

robin straight cath, then if still having issues= antihypertensive &

anticholinergic

Guillain-Barre (1): de-mylination of the myelin sheath of

neurons 2

nd

to a viral infection, flu-shot, etc.-decreases or

takes away muscular control; the immune system produces

harmful antibodies that attack the nerves; assymetrical

Has a specific pattern: starts at the feet (bilaterally) and

works up =feet start to plantar flex-fixed plantar flexion

(paralysis), they are unable to dorsa flex—if it is not stopped

then will continue up & once it hits the diaphragm then they

must be ventilated-can no longer breathe

TX: daily infusions of IVIG (intravenous immunoglobulin)-comes from

donated blood w/ healthy antibodies

Assessment initial SCI (1): airway= spinal shock-nervous system

stops working initially; bag or ventilate right away-will be

intubated Spinal shock= can’t move, can’t breathe and can cause

neurogenic shock-SNS is diminished at first=system wide

vasodilation=causing hypotension and bradycardia (low CO-cardiac

output)

Head to toe, VS, digital stimulation of the bowels, positioning

ALS (amyotrophic lateral sclerosis) (1): Lou Gherig’s disease

They have musculature issues, but resp. failure is are most important concern

AFFECTS the spinal cord

TX: riluzole and edaravone-reduce damage to motor neurons by decreasing the

levels of glutamate, which transports messages between nerves and motor

neurons

SCI level>C6 (1): C6 and above, are very important; C4

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