GI-PART 2 Lecture for RN

8/8/2019 GI-PART 2 Lecture for RN

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PART 2 GI PATHOLOGY: LIVER, PANCREAS, & BILIARY SYSTEMFUNCTIONS OF THE LIVER:Dr. ROXAS ± September 28, 2010

- Has cells called HEPATOCYTE

a. Necessary for metabolism stuff

b. Erythropoiesis

- During Intra-utero (2nd trimester) the liver & spleen is capable of

producing RBC. (Yolk sac 1st trimester, 3rd trimester-birth (Bones) )

- During CHRONIC ANEMIA ex:

1. Cancer elevation of TNF alpha that my inhibit erythropoietin release

2. Hemoglobinopathies (thalasemia)

- The liver & spleen hyperplasia HEPATOSPLENOMEGALY these

organs has capability of producing RBC.

c. Storage

1. Blood supply stores - Acute blood loss Liver & Spleen contracts stored blood adds on the blood volume that has been during the

hemorrhage. Therefore there no change in the serum of RBC, Hct level but

there is loss in the blood volume.

2. Glycogen stores ± Excess glucose or energy derived from amino acids

or fats stored energy in the liver. During of starvation these glycogen can

be converted to Glucose as a source of energy.

3. Adipose/Fats Pathological changes (fatty change), alcoholism

&hyperlpedemia.

d. Synthesis of Bile. Cholesterol, energy etc

.

Macrophages (Kupper Cells)

RBC sequestrated by the spleen HEME + GLOBIN

HEME BILIVERDIN (Will further synthesized by liver) + Fe++ (Transported

back by iron binding CHON / Transfferin to the Bone marrow)





ROLES LIVER

1. HemeOxygenase (HEME BILIVERDIN)

1. Biliverdinreductase (BILIVERDIN BILIRUBIN unconjugated)

2. UDP Glucoronidetransferase (Unconjugated lipid solube (not readily

excreted Conjugated water solute not easily absorb readily excreted in the

urine, feces)

a. Immunogenic actions to immunogens (bacteria/virus/fungal/parasites)

b. Degradation of HEME or damaged RBC (SPLEEN) reticuloendothelial

system (is already the job of hepatocyte) Biliverdin (Bilivervinreductase

BILIRUBIN unconjugated)

c. Enzymes that induce apoptosis to the hepatocyte

Bilirubin > 300mg in times of hyperbilirubinemia KERNICTERUS (CNS Damage),

Jaundice

1. Massive RBC Destruction

2. Liver disease obstruction in the portal tracts



General functions of the Liver:

1. Involved in Major Metabolic Processes.

a. Cytochrome p450 system necessary for drug metabolism

b. Carbohydrate Metabolism

- Glycolysis Storage Glycogen (major site) glucose

- Gluconeogenesis Using non-glucose source (CHON amino acids & FFA) can

be used to form Acetyl-CoA (for Kreb Cycle)

- Conversion of Fructose to glucose (Pentose Phosphate Pathway)

2. ALBUMIN PRODUCTION Proteins is a complex type amino acids (LIVER)

a. Osmotic Pressure Regulation (Intracellulary) Resist Hydrostatic pressure

so that fluids in the extracellular will not move inside cell PREVENT 3rd

spacing or edema.

b. Drug Binding bound drugs to protein are inactive form (high protein bound

drugs) NO PHYSIOLOGICAL ACTION

Neonates IMMATURE LIVER Less or no albumin

ELDERLY LIVER DEGENERATED/ damage Less albumin

Drugs should not be same dosage as in normal functioning liver adult

OVERDOSAGE OR POISONING

c. Can serve as energy reserve in times starvation NET PRODUCT KETO ACIDS

c. Protein Metabolism

ALL PARTS IN YOUR BODY contain the following enzymes: Found inside

the cytoplasm of the cell, actions is deaminating the amino acids(PROTEINS)

1. Aspartate aminotransferase/ SGOT/AST GLUTAMINE alpha

KETOGLUTARATE (PART OF THE KREB CYCLE ATP production)

2. Alanine aminotransferase/SGPT/ALT PYRUVATE (KREB CYCLE )

ENERGY

Deamination of CHONs NH3+ (AMMONIA)

- CO2, Alcohol, NH3+ PASS THROUGH cell membrane freely EASILY

ABSORB.

- AMMONIA is converted by the liver via ORNITINE CYCLE/ UREA CYCLE

UREA (Excreted in the feces & urine)

1. Can produced conversion of UREA into ammonia by Intestinal bacteria

(UREASE)



- can be prevented by NEOMYCIN (Kills microorganism), LACTULOSE

(Osmotic Diarrhea) MAITAE and lactic acid that formed prevents urease

activity.

- Remember if the PORTAL CIRCULATION is obstructed/ PORTAL

HYPERTENSION F ormation of collateral venous system by pass the liver

Ammonia cannot go directly and covert to urea level of ammonia rises in

the blood HYPERAMMONEMIA

- Degradation of Purine & Pyrimidine Amino Acids UREA NH3 (INTESTINE)

- Remember: NH3 is highly lipophillic it can pass through cell membranes, this can

be reabsorbed & also can penetrate the Blood Brain Barrier CNS

- If you have too much NH3

1. Encephalopathy (Hepatic) Damages the cell membranes of the nerves that

Impedes the synaptic homeostasis (Electrical & Chemical) (RELATED IN LIVER

FAILURE)

RATIONALE: HYPERAMMONEMIA there conversion of direction reaction toGLUTAMATE FORMATION INHIBITS FORMATION OF alpha KETOGLUTARATE

KREBS CYCLE REDUCED LACK ATP LACTIC ACIDOSIS ISCHEMIA death cell

CNS. COMATOSE

1.bCan cause bubbles (this is not related to LIVER FAILURE DEEP SEA diving

(Barotrauma BENDS can cause embolism & Stroke) if very fast ascending from the

deep sea. (DIFFERENT STORY)

- Transamination of Proteins

d. FAT Metabolism- Cholesterol Synthesis of (VLDL & HDL)

- Bile is formed Emulsify Fats in the Ileum area To form Micelles bind in the

lacteals Thoracic or Lympathic duct in the circulation.

- Bile Fat Soluble Vitamins absorption (ADEK)

e. For the conversion of ANGIOTENSINOGEN AGIOTENSIN 1 (aided with

RENNIN release by JG CELLS of the afferent arteriole of the Kidney)

2. Synthesis of Proteins:

Albumin Production Characteristic Action:

- Regulation of Osmotic Pressure ( Resistance to the Hydrostatic Pressure)

- Drug Binding (Protein Bound Drugs NO PHYSIOLOGIC EFFECT)a. Drugs

b. Fe (Iron Binding Protein)

c. T3 & T4 (Thyroxine Binding Protein)

Therefore all unbound drugs these participates on Physiologic Actions.

- The albumin is also the measure for (Nutrition in the body specially in patients

with PEM)



3. Synthesis of Clotting Factors for Control of Bleeding: (II, VII, IX, X 1972) with

the action of the Vitamin K

4. Synthesis of Fat Soluble Vitamins

a. (EXAMPLE) Step in initial activation of Vitamin D2 Vitamin D3 (KIDNEY)

5. For the Synthesis of Globin Molecule Immune-response ( Immunoglobulin in

Humural Immunity *(IgG, IgA) IMMUNO+GLOBIN

Unconjugated Bilirubin Increase

1. INBORN ERRORS of Metabolism ( NO BILIVERDIN REDUCTASE or NO

UDP-GT)

2. SUPER DAMI ng HEMOLYSIS (destruction of RBC)

- BLOOD TRANSFUSION RXN

- IMMUNE RESPONSE (AUTOIMMUNITY) SELF DESTRUCT

- INFECTION (MALARIA)

- ANIMAL TOXIN (VIBURA LOYAL SERPENT OF VALENTINA COBRA)

- SPLENOMEGALY (LUMAKI ang SPLEEN) Increases the size, enzymaticactivity of the Reticulo endothelial cells HIGHER FUNCTION DESTRUCTION

RBC

- GENETIC (Thallasemia, Membrane Defect)

- Mechanical ( Prosthesis MITRAL VALVE ARTIFICIAL ) cause damage directly

in the RBC HEMOLYSE

- Mechanical FORCE or COMPRESSION SINAPAK, INIPET, NECROSIS,

decrease blood flow

a. Conjugated Bilurubin Increased

- VERY COMMON (LIVER CIRRHOSIS) specially if (+) FIBROSIS of the

Hepatocyte (OBSTRUCTION OF THE BILIARY SYSTEM)- STONE in the Biliary Tract

- Strictures ( kumipotung BLOOD VESSEL NG PORTAL CIRCULATION

atherosclerosis)

- TUMOR Compression

- GENETIC

5. STORAGE of BLOOD: MAJOR (400ml?)

6. STORAGE of MINERALS & VITAMINS (IRON)

7. PORTAL SYSTEM MAJOR BLOOD FLOW & Control of Pressure

CONSEQUENCES IF THERE IS (+) LIVER DAMAGE

1. Impaired Metabolism

2. Bleeding 10,9,7,2 inhibition

3. Obstruction to flow PORATL CIRCULATION



v



4. PORTAL HYPERTENSION

- Obstruction Portal Tracts COLLATERAL CIRCULATION



a. Esophageal Varices (Block L gastric Artery)

- This can generate the following symptoms:

1. Odynophagia usually after swallowing specifically solid bolus

2. Dysphagia with solid foods can be relieved significantly with water/liquids

3. Angina Pectoris but non cardiac origin

4. Vomiting can cause pressure in the esophagus that can mimic esophageal

venal rupture.

b. Gastric Ulcer Blockage to the blood flow and reflux may complicate

symptoms including esophageal damage

c. Rectal Varices notable blood in the anal area or after defecating. Must

institute laxatives to prevent straining or valsalva maneuver

d. Umbilical Varices Caput medusa

e. Peritonitis or enlargement of the abdomen

5. Hypoalbuminemia EDEMA (3rd Spacing), due to osmotic pressure reduction vs.

hydrostatic pressure

- Important to modify salt, NSS, water intake may retain cause hypervolemia

6. Vitamin Deficiency ± ADEK- Vitamin A May precipitate vision complaints, and reduction of growth of mucous

membranes

- Vitamin D May rise serum levels of calcium in the blood due to leaking out of

calcium in the bone and may be excreted in urine and feces

- Vitamin K Complicates bleeding

7. Immunosuppression

8. Hypertension PORTAL CIRCULATION& Collateral circulation, back-flow

-must remember that portal obstruction mediated by fibrosis of liver may impede

ammonia flow from the blood preventing ammonia (usually from intestines due

urease mediated bacterias) to proceed ornithine cycle/urea conversion

9. Accumulate NH3 CNS inflammation (increase cell membrane permeability

damage Decrease neurotransmitter release, impaired synapsis HEPATIC

ENCEPHALOPATHY (Coma Late & very high ammonia in blood), Hepatic Flap

& Apraxia, even behavioral changes early)

- Remember that alpha ketoglutarate may not give the CNS enough energy ATP,

that may activate lactic acidosis and damage.

10. Metabolic Acidosis Lactic acid buildup.

11. FATS

Cholesterol

REQUIREMENT in steroid synthesis(affect ESTROGEN GYNECOSMASTIA (FOR MALES only, estrogen fails to converted to

testosterone), CAPUT MEDUSAE

12. HEPATO-RENAL syndrome Renal failure in Liver Failure (Remember this is

transient if LIVER failure becomes compensated this can be recovered) Related

to decreased renal blood flow RENNIN RELEASE VASOCONSTRICON

Reduction in blood flow in the kidney that may damage kidney.



- Check the urine output is very critical (0.5cc/kg/hr)

CAUSATIVE AGENTS:

1. CHEMICAL (Drugs hepatotoxic, Alcohol, AFLATOXIN (Nuts) fatty liver,

Benzene)

2. BIOLOGICAL (Atherosclerosis in the portal tracts,Hyopercholesteremia,

Obstruction stones, Parasite, Strictures, Viral hepatitis, Parasites, Bacterial)

3. IMMUNOLOGICAL (Autoimmunity)4. DEGENERATIVE (old age, senescence cells apoptosis reduce number of

hepatocytes reduction function)

5. CONGENITAL (Inborn errors, Atresia)

6. MECHANICAL (Gunshot, Bugbug, Tumor, etc)

7. GENETIC

8. PARASITES (Liver Fluke &Amoebiasis)

9. INFECTION: Hepatitis B (10-20 Years), & C (faster)

LIVER CIRRHOSIS: Irreversible liver damage (accumulation of regenerative

cells, inflammatory substrates , collagen type 1 & FIBROSIS), last stage of changes in the liver.

Changes on how the liver adapt on the insults:

1. Fatty Changes Phase

2. Hepatitis/Inflammatory Phase

3. Cirrhosis of the Liver Phase

4. Liver Failure

5. Hepatocellular Carcinoma (Cancer)

Etiology:

A. Alcoholic (common) or Laennecks Cirrhosis

B. Cryptogenic (Unknown cause) Cirrhosis

C. Drug-Induced Cirrhosis (Chemotherapy)

D. Cardiac Cirrhosis R Sided Heart Failure

E. Posthepatitic (portal tracts)

- Presinusodal Portal Tracts (SVC/IVC) ± problems Strictures or damage in the

blood vessel, Shock or loss blood)

- Sinusodal Within the hepatocyte (Viral (Hepatitis C & B), Enzymatic Free

Radical Damage, Parasitic, Alcoholism etc)- Postsinusodal Biliary Tracts (Gallstones, Pancreatitis etc)

F. Inherited

G. Parasities

Insult in the hepatocyte damage in cell membrane Inflammation released

(Pholipase A2, Leukotrine Synthesis, Arcachidonic Synthesis, PGE1, etc)



Leukocyte migration and Differentiation (KUPPER CELLS) releases Cytokines

(TNF alphaLeukocyte differentiation, damage, TGF B (Collagen Type1),

IL1(FEVER), IL6) Changes in the structure FIBROSIS LOSS FUNCTION

Dysfunctional Changes in Liver Cirrhosis:

a. Anorexia

- (TNF-alpha) (controls the satiety center)

- Accompanied with Hepatomegaly or Ascites can cause compresses the

stomach fullness feeling (BUSOG)

- Dysphagia ( related to the Esophageal Varices Obstruction on the bolus

flow)

b. Malnutrition (loss of albumin formation, Loss of synthesis & storage of Fat

soluble vitamin (ADEK) & Carbohydrate Metabolism (Hexokinase,

Glucokinase etc. are affected)

c. Easy Bruising (Loss synthesis of Vitamin K Coagulative problems X, IX, VII,

II synthesis)

d. Easy Fatigability Carbohydrate Metabolism is affected( production of ATP,

doesn¶t satisfy the need body weakness)e. MALE Hormonal ImbalanceGynecomastia (breast enlargement), Palmar

Erythema, Caput Medusa, Testicular Atrophy ( PERIPHERAL ESTROGEN

CONVERSION accumulation ANDROSTENEDIONE ) (because unable

degrade

f. PORTAL HYPERTENSION Obstruction in the tracts that govern the portal

system ( Because of compression, obstruction of fibrosed hepatocyte)

Effects of PORTAL HPN: is not HIGH BLOOD focus



NORMAL 5-10mmHg

ABNORMAL >10mmHg

Obstruction to flow (because of the fibrosed hepatocyte due to compression)

Generates pressure> 12mmHg Reduction in the portal blood flow

a. (some areas of the hepatocyte can be ischemic)

b. Porto-Fugal Flow Formation of Collateral Circulation ( Back Flow in

areas has less pressureVEINS)

1. GastrioesophagealVarices (Cardiac-Esophageal Junction) Bleeding

(ulcer, rupture) Risk

2. DANGER RUPTURE BLOOD LOSS SHOCK

3. Esophageal Varices precipitate Dysphagia (obstruction & decrease in

the diameter of the esophagus)

ESOPHAGEAL VARICES Treatment:

a. Vasoconstrictors (VASOPRESSION/IV)Vasoconstrict the blood

vessels RISK Ischemia & HPN

b. REPLACEMENT BLOOD (if (+) Blood Loss), Lactate Ringers

INVASIVE PROCEDURES CONSENT: REQUIRES SEDATION

c. Endoscopic Banding

d. Endoscopic Sclerotherapy injects (?)

e. BaloonTamponade

- SENGSTAKEN BLAKEMORE (3 LUMEN)



- MINNESOTA (4 LUMEN)



- Endotrachial tube should be inserted risk aspiration (saliva)

- Side Effects: Esophageal Ischemia or Necrosis REDUCED BLOOD FLOW in

the Esphageal Mucosa (Arterial Compression) Perforation or Damage in

Esopgaus

- If survived , Risk for Esophageal Strictures & Fibrosis

- ACTIVE ESOPHAGEAL BLEEDING: EMERGENCY & DEADLY

a. Reduce of Blood Pressure SHOCK

b. CNS signs: Dizziness, Seizure,Delerium Reduction of Cerebral Blood Flow

c. Tachycardia Arrhythmia ( Baroreceptor Reflex)

4. Rectal Varices Hemorrhoids & Bleeding

- AVOID (VALSALVA MANEUVER or Straining) rupture

- GIVE Laxatives Lactulose Easy Defecation

- DO NOT LABATIBA BAKA MATUSOK AT PUTOK ANG UGAT RECTUM

5. Jaundice - Due obstruction portal tracts

- Failure to convert conjugated bilirubin DAMAGED HEPATOCYTE

- Accumulate conjugated bilirubin OBSTRUCTION

- HEMOLYSIS Toxins etc.

EFFECTS:



a. Itchiness or Skin irritation ACCUMULATION of BILE PIGMENTS

b. Eyes Irritated in some cases (Inflammation by inflammatory cytokines)

FOREIGN BODY Bile pigments

c. DANGER if the Bile is severe sp. Unconjugated KERNICTERUS

- Monitor serum levels of Bilirubin, dialysis might be an option

6. Ascites

a. No albumin (lack of production) Loss of Oncotic Pressure

b. Increase in Intra-hepatic Pressure (obstructed portal tracts)

pushes the fluid towards peritoneal area

c. Aldosterone Release (Adrenal Cotex)(Decrease Renal Blood Flow

ANGIOTENSIN 2 activation to AT1 receptor) Na & waterretention

(Collecting Tubles)

Effects:

a. Anorexia Mechanical Compression to the Stomach

b. Dyspnea Compressive Effects that obstructs the ventilation

process (Compressive Type Atelectasis Risk Collapse Lung)

affect CO2 Risk for acidosisy 3types: Compressive (Ito angsa ascites okay), Obstructive,

Contractive

c. Mobility Deficit Daily chores are affected

d. Bain Bridge Reflex Activation (increased water retention

increasing blood volume) Tachycardia (Increasing work load on

the heart) Cardiac Remodeling (Hypertrophy or ACS Acute

Coronary Syndrome)

e. Increase work load kidney Release of RENNIN Vasoconstriction

by (ANGIOTENSIN II) RENAL BLOOD BLOW decrease U/O or

ARF (HEPATO-RENAL-FAILURE or SYNDROME)

Treatment:

1. Glucorticoids Reduces Inflammation

2. Furosemide (LASIX) (LOOP) or Spironolactone (K-sparing

diuretic)

3. NaCl restriction & water intake(modify) Aldosterone release)

4. Monitor the weight & size of the abdominal girth

- With the use of Furosemide enhancing K loss pH rises (risk NH3 formation

HEPATIC ENCEPHALOPATHY)

- So K-sparer prevents K loss lowers the pH Reduces the risk rising the NH47. Encephalopathy Entry of ammonia in the cell membrane (CNS) this

damages the depolarization that impedes synaptic response.

AMMONIA LIPOPHILLIC it can pass through the cell membranes , and readily

reabsorbed.

What are the incidences to Rise your NH4:



1. Protein Intake (monitor diet) Came from CHON degradation forms NH4

2. Colonic Bacteria produces NH4 specially in the presence of CHON

Treat:

- Providing ANTIBIOTIC : NEOMYCIN (non absorptive antibiotic) reduce the

number of colony of bacteria

- Providing use of Osmotic Laxative: L ACTU LOSE (Colonic bacteria will not

produce NH4 because this decreases GI pH (LACTIC ACID)

- Providing BENZODIAZEPINE (Flumazepine)GABAmimetic (UMAYOS ANG

UTAK wag moinumin please)

3. Bleeding GI tract (amino acids/CHON in RBC or blood rises NH4)

4. Rise pH

5. Loss Potassium or Hypokalemia ( using LOOP diuretics)

- ABG should be monitored for pH (rise pH indicates NH4 formation)

- Pulse oximeter check PaO2 & PaCO2

Stages Encephalopathy:(+) ASTEREXIS FLAPPING TREMOR because

un-synchronous depolarization nerve fiber)

STAGE 1: Euphoria

STAGE 2: LethargySTAGE 3: Confusion

STAGE 4: COMA permanent damage (-) ASTEREXIS

6. HEPATOMEGALY

7. SPLENOMEGALY (Splenic vein Collateral) RAS activation by kupper cell

Destroys the RBC HEMOLYTIC ANEMIA

8. ANEMIA cause:

a. SPLENOMEGALY Destruction of the MORE RBC

b. VARICES RUPTURE

c. ULCER STRESS

d. LOSS CLOTTING FACTORS (Vitamin K synthesis) RISES prothrombin

time

e. Loss of Vitamin (Folic Acid metabolism, ADEK)

f. TNF alpha inhibition of Erythropoietin release (KIDNEY) ANEMIA of

CHRONIC DISEASE

Diagnostics:

Blood chemistry: AST, ALT, Cholestrol, NH3

Biopsy

Cirrhosis (beneficial for patients who deny alcoholism)Ultrasound

MRI

ALCOHOLIC LIVER CIRRHOSIS:

Ask bottle/day, years, when is the last time?

- Considered to be malnourished (loss of Vitamin B6, & 12)



- Amount of Alcohol & Length EXPOSURE (years)

- Most common cause of liver damage (M>F common) but Females is most

affected has greater damage

- 1 BEER (330ml) 12g/dose of alcohol

- 60-80g/d for 10 years of exposure CIRRHOSIS

Changes of Liver Hepatocyte Architecture with Exposure HEPATOTOXIN:

STAGES

a. Fatty Liver (REVERSIBLE) accumulation of fatty lobules, 40-60g/d

b. Alcoholic Hepatitis Inflammation

c. Liver Cirrhosis (IRREVERSIBLE) Collagen type 1 substrates & Fibrosis +

Regenerative cells, if there is changes in the structure function

changes,also (loss). (Cytokine release TNF ±alpha, Transforming Growth

Factor Beta (TGF Beta) Collagen Type 1, IL1, IL6) , 80-160mg/d (alcohol)

d. LIVER CANCER (Hepatocellular Carcinoma)

(GALL BLADDER) Cholelithiasis STONE

- OBESITY (Accumulation of FATS & Cholesterol)

- Weight Loss (* Anti-fat etc.) (Accumulation of Free Fatty acids in the Biliary

Tracts)

- FEMALE (Estrogen Surge Retention of Cholesterol & FFA)

- PREGGY Compression in the Gallbladder HYPOMOTILITY ( loss of

peristaltic movement SLUDGING)

- OLD AGE (HYPOMOTILITYStone sludging)

REMEMBER: Risk for Pancreatitis & Liver Damage

1. Pancreatic Damage is due when the stone obstructs the common biliary tract that

increase pressure in the pancreatic duct (Pancreas secretes zymogens, bicarbonate

and pancreatic amylases May add build up pressure May compress effect the

following:

1. Zymogen can be activated AUTODIGESTION Damage

2. Pressure can compress pancreatic arterial system that may decrease blood flow and pancreatal lactic

acidosis Damage

2. Liver failure May damage the liver due pressure.

STAGES STONE FORMATION

1. Supersaturation (Accumulate Cholesterol)

- Rises the nucleation ( MUCUS &Cholestrol)

- Lowers the nucleation (Lecithin, APO-1)



2. Nucleation

3. Microstoning formation

4. Stone Formation BILE PIGMENT (CALCIUM)

CONSEQUENCES: STONE FORMATION

1. Stone generates pressure Increase in the gallbladder Intra-luminal pressure

dilatation

- Compress mucosa (dilation & stretch), and arteries that supports the gallbladder

reducing cholecystal blood flow Ischemia Inflammation Necrosis

Perforation

2. Stretching the gall bladder induces reflex

contraction of gall bladder

NOCICEPTOR activation Biliary COLIC Pain

3. Obstruction in the Biliary Tracts risk for damaging the liver (Posthepatitic),

Pancreas Obstructs the enzymatic flow in the common bile duct area that lead

to autodigestion of enzymes due to pancreatic enzyme back flow( cause

inflammation to the pancreas)

4. Generates infection (stone) Anaerobes

Symptom:

1. Cytokine Release : (non-specific)

TNF alpha Nausea & Vomiting CTZ activation

IL1 FEVER

2. PGE2 release (Phospholipase A2 A.A), Bradykinin NOCICEPTOR

ACTIVATION VICERAL PAIN, Contraction Reflex COLIC PAIN

(RUQ)

3. RARE Steatorrhea (FULL BLOWN OBSTRUCTION NO BILE RELEASE)

4. JAUNDICE (FULL BLOWN OBSTRUCTION)



Diagnostics:

ULTRASOUND

Abdominal Xray

TREATMENT: Surgery

1. Cholecystectomy

2. Laparoscopic Surgery

Non-invasive Ultrasonic device

Cholecystitis Inflammation

- Stone

- Parasites

- Viral

- Compression

- Immune Mediated- Ischemia Reduction in the Blood flow

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GI-PART 2 Lecture for RN

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