Final REVISED Final Exam Study Guide Patho Spring 2022, Exams of Health sciences

Final REVISED Final Exam Study Guide Patho Spring 2022

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Final REVISED Final Exam Study Guide Patho Spring 2022
Final Exam Concept Guide
Know the Etiology, Signs/Symptoms, Diagnosis/Diagnostics, Clinical
Manifestation, Risks, Treatment and Complications for the following:
Gastritis
Gastritis – inflammation of the stomach lining
Acute Gastritis – (just acquired) ingestion of toxins, alcohol, aspirin or other
irritating
substances
Chronic- 2 months to become chronic
Triggers of Gastritis: Alcohol, caffeine, autoimmune disease, viral or
bacteria Chronic Gastritis: H Pylori is always a factor
H Pylori goes very deep in the lining of the stomach and It causes persistent
inflammation
S/S: N/V – Anorexia- postcranial discomfort
Post Cranial Discomfort- after eating- goes away and come
back 1-2 hrs Gastritis- hematemesis- blood in the vomit- coffee
brown color
Treatment: Treat H pylori treat GERD, change lifestyle, PPI
Peptic Ulcer Disease
Inflammation and ulceration in the stomach (acid and
pepsin) Gastric: stomach location
Duodenal: duodenal location
PUD is a complication of
Gastritis
PUD is caused by aspirin, H pylori, Nsaids, Stress,
Smoking
S/S Gastric N/V Anorexia Chest discomfort,
asymptotic, Dyspepsia
Duodenal – normal weight
Biggest complication of PUD- GI bleeding due to Ulcer perforation- hole in
the lining and bleed
It is life-threatening if it keep bleeding (Anemic, electrolytes imbalance (losing
volume) Duodenal – Blood in the stool – black and tarry
Bleeding profusely-frank with
cloth Hematemesis- Bleeding in
vomiting
Treatment: Cortery of perforation, treatment of H. pylori, PPI, Cessation of smoking
Ulcerative Colitis and Crohn’s the difference in the
complications
Complication in UC Malnutrition – dehydration, increased
risk factor of colon cancer
7-10 yrs, rarely in megacolon
Complication of Chron- Fistulas, perianal fissures, abscesses. The risk of colorectal cancer
Bowel Obstruction Manifestations
Obstructions in the jejunal area: Vomiting, dehydration, electrolyte depletion
Obstructions of the distal portion of the small bowl or ileum, dehydration to
hypovolemic schock
Obstructions of the colon: Massive gas distention
Blockage of the colon by a tumor is the most common cause of colonic obstruction
and perforation of the bowel wall adjacent to the tumor.
What percentage of the pancreas is dedicated to endocrine functions?
Only 5%
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Final Exam Concept Guide Know the Etiology, Signs/Symptoms, Diagnosis/Diagnostics, Clinical Manifestation, Risks, Treatment and Complications for the following:Gastritis Gastritis – inflammation of the stomach lining Acute Gastritis – (just acquired) ingestion of toxins, alcohol, aspirin or other irritating substances Chronic - 2 months to become chronic Triggers of Gastritis: Alcohol, caffeine, autoimmune disease, viral or bacteria Chronic Gastritis: H Pylori is always a factor H Pylori goes very deep in the lining of the stomach and It causes persistent inflammation S/S: N/V – Anorexia- postcranial discomfort Post Cranial Discomfort - after eating- goes away and come back 1-2 hrs Gastritis- hematemesis- blood in the vomit- coffee brown color Treatment: Treat H pylori treat GERD, change lifestyle, PPI ▪ Peptic Ulcer Disease Inflammation and ulceration in the stomach (acid and pepsin) Gastric: stomach location Duodenal: duodenal location PUD is a complication of Gastritis PUD is caused by aspirin, H pylori, Nsaids, Stress, Smoking S/S Gastric N/V Anorexia Chest discomfort, asymptotic, Dyspepsia Duodenal – normal weight Biggest complication of PUD - GI bleeding due to Ulcer perforation- hole in the lining and bleed It is life-threatening if it keep bleeding (Anemic, electrolytes imbalance (losing volume) Duodenal – Blood in the stool – black and tarry Bleeding profusely-frank with cloth Hematemesis- Bleeding in vomiting Treatment: Cortery of perforation, treatment of H. pylori, PPI, Cessation of smoking ▪ Ulcerative Colitis and Crohn’s the difference in the complications Complication in UC Malnutrition – dehydration, increased risk factor of colon cancer 7-10 yrs, rarely in megacolon Complication of Chron- Fistulas, perianal fissures, abscesses. The risk of colorectal cancer ▪ Bowel Obstruction Manifestations Obstructions in the jejunal area: Vomiting, dehydration, electrolyte depletion Obstructions of the distal portion of the small bowl or ileum, dehydration to hypovolemic schock Obstructions of the colon: Massive gas distention Blockage of the colon by a tumor is the most common cause of colonic obstruction and perforation of the bowel wall adjacent to the tumor. ▪ What percentage of the pancreas is dedicated to endocrine functions? Only 5%

Pancreatic Cancer Pancreatic Cancer – 2% of all cancers Ranked 4 th^ among death in all malignancies Risk Factors; cigarette smoking, obesity S/S; head: Jaundice, malabsorption, weight loss tail: Abd pain, nausea’ ▪ Hepatic Encephalopathy is due to? Hepatic encephalopathy is a decline in brain function due to severe liver disease

and treat anemia Improve quality of life Lower mortalty and morbidity rates Control pains VS RISKS Electrolytes imbalance (potassium and sodium) -need to check hyper or hypo

Low blood pressure (have to check vitals before and after) Risk for infection Long-term mobidity Life threatening Cardiovascular disease remained the most common cause of death in ESRD patient ▪ Acute Kidney Injury- Three phases- Prodromal- Oliguric- Postoliguric Prodomal Phase

  • Normal or declining urine output
  • Serum blood urea nitrogen (BUN) and creatine levels rise Oliguric phase (10-14 days) range from 1 day to 8 weeks
  • Oliguria – Small abnormal amount of urine
  • Edema, Hypertension, Hypervolemia
  • Distended neck veins, weight gain
  • Crackles, possibly heart faily
  • WBC and RBC in urine
  • Protein in urine
  • Hyperkalemka
  • Volume overload
  • Azotemia and uremia
  • Metabolic acidosis Postoliguric phase (5% recover)
  • Fluid volume deficit
  • Labs begin to normalize
  • Polyuria – sodium waste ▪ ▪ Acute Tubular Necrosis and the causes of Acute Tubular Necrosis ATN is the result of tubular cell injury
  • Ischemia: Exposure to nephrotoxic substances
  • ½ of all cases of AKI Nephrotoxins leading cause of ATN (aminoaglycosides, NSAIDS, amphotericin B, cisplatin, tetracycline. CI- AKI or Contrast-induced nephropathy ▪ Cystitis- signs and symptoms (inflammation of the bladder) no fever or flank pain If fever is present – Might be infection (UTI) Confusion Cloudy urine Frequency Urgency Dysuria Intrarenal Kidney Injury- Toxic causes of Box 28. Types of Acute Kidney Inj ury Prerenal

o • Distributive shock (neurogenic, anaphylactic, septic) o • Third-spacing and edema o • Decreased cardiac output ▪ • Cardiogenic shock ▪ • Dysrhythmias ▪ • Cardiac tamponade ▪ • Heart failure ▪ • Myocardial infarction

  • • Primary renal hemodynamic abnormalities o • Occlusion or stenosis of renal artery* o • Drug-induced impairment of renal autoregulation in susceptible persons† Postrenal
  • • Benign prostatic hyperplasia
  • • Kinked or obstructed catheters
  • • Intraabdominal tumors
  • • Strictures
  • • Calculi Intrarenal/Intrinsic
  • • Tubular (acute tubular necrosis) o • Ischemic ▪ • Prolonged prerenal failure ▪ • Transfusion reactions ▪ • Rhabdomyolysis o • Nephrotoxic ▪ • Prolonged postrenal failure ▪ • Certain antimicrobials (antibiotics; antifungal and antiviral drugs) ▪ • Radiographic contrast media ▪ • Certain cytotoxic chemotherapy agents ▪ • Recreational drugs (amphetamines, heroin) ▪ • Environmental agents (heavy metals, carbon tetrachloride, insecticides) ▪ • Snake and insect venom
  • • Glomerular o • Acute glomerulonephritis
  • • Interstitial o • Acute allergic interstitial nephritis o • Acute pyelonephritis
  • • Vascular o • Vasculitis o • Emboli o • Nephrosclerosis (due to primary hypertension, hypertensive emergencies, and urgency) ▪ ▪ Two electrolytes that are affected by the kidney’s inability to regulate. Potassium and Sodium Hypokalemia and Hyponatremia ▪ Renin-Angiotensin-Aldosterone System and the relationship

between the autoregulation of the kidneys Renin-Angiotensin-Aldosterone System (RAAS) act to increase the total circulating volume in the kidney attempt to autoregulate perfusion and maintain GFR.

➢ Traumatic brain injury == head injury ➢ Injuries to the cranials ≠ not always brain injury ➢ TBI is the leading cause of death and disability in the U.S. 50,000 + yr ➢ Causes TBI (falls, sports injuries, firearms, and transportation-related trauma) ➢ Fall majority for 0-4 or 65+, motor vehicle TBI – 14-24 yr. Men are more likely to die than women ➢ Types of TBI: ▪ Severity ▪ Location ▪ Mechanisms of injury

➢ Severity of TBI is classified by Glasgow coma scale (CGS) (standardized tool developed for the purpose assessing the LOC in acutely brain-injured patients. To evaluate patient with an altered LO ➢ Glasgow coma scale: Mild score (13-15), Moderate (9-12), severe (8 – below) ➢ Primary injury- initial trauma injury on brain cells

- Focal injuries (coup)

- Polar injuries (coup contrecoup)

- Diffuse injury

In addition, as location, Primary Injury can also differentiated by Mechanism of injury

- Concussion

- Contusion

- Intracranial hematoma.

Concussion also known as Mild traumatic brain injury (MTBI) most common for military and athletes. Alterations or LOC≤30 mn but no evidence of brain damage on CT. Symptoms: Headache, n/v, dizziness, fatigue, blurred vision, cognitive, emotional disturbances Contusion CT or MRI reveals area of Brain Tissue damage (necrosis, laceration, bruising) Intracranial hematoma: Localized collection of blood within the cranium. Three types; Epidural, subdural, subachnoid. Secondary Injury : Body’s response to initial injury may cause more harm than the initial injury. Can cause: Ischemia, hypoxic events, vasogenic/neurogenic edema, and other processes that leads to brain swelling and increased ICP. Treatment: Cardiopulmonary stabilization. Radiologic screening, maintenance of normal body temperature or mild hypothermia, normal PaCO2, normal glucose level and noema intravascular volume recommended. Acutely elevated ICP, mannitol(osmotic diuretic) sedation, hypothermia and mild hyperventilation. ▪ Reperfusion Injury- Definition Reperfusion injury is the secondary injury that occurs after reestablishing blood flow ▪ Increased Cranial Pressure- ICP ▪ ICP is the pressure exerted by the contents of the cranium and normal ranges from 0-15 mmhg The volume of the cranium nerve is made up 3 parts: brain tissue, cerebrospinal, blood Monroe-kellie hypothesis – the relationship between the 3 components of cranium Compliance – the ability to accommodate changes in volume w/o sign. Increase in pressure The most common causes of ICP: stroke, trauma and tumors ▪ Most sensitive indicator of altered brain function? A change in Level of consciousness LOC is one of the most sensitive indicators of altered brain function ▪ Assessment of the brainstem function- How do you assess it? Pupil light reflex Oculovestibular reflex Corneal reflex ▪ CVA- Types and causes

Hemorrhagic stroke = Hemorrage within the brain parenchyma and after a severe and long- standing Hypertension. (30 % mortality rate) ▪ Test used to diagnosed CVA Non-contrast CT scan /diffusion weighted brain MRI ▪ Meningitis what is it? Meningitis is the pyogenic infection that invades the leptomeninges and the subarachnoid space. the most comment sequela to microbial invasion of the CNS. (most bacterial but can be viral/fungal) Bacteria: Streptoccocus pneumoniae ▪ Encephalitis What is it? Encephalitis is the inflammation of the brain caused by viruses, bacteria, fungi and parasites ▪ Seizures- how they are classified?

  1. Generalized seizures: Entire brain Surface
    • Absence (petit mal)
    • Atypical absence
    • Myoclonic
    • Atonic (drop attack)
    • Clonic
    • Tonic
    • Generalized tonic-clonic (grand mal)
  2. Partial Seizure: Part of the brain surface
    • Simple partial: There is no impairment of consciousness during the seizure.
    • Complex partial: There is impairment of consciousness during the seizure.
    • With secondary generalization: Onset begins as simple partial and then progresses to impairment of consciousness. ▪ Status Epilepticus what is it? Status Epilepticus is a continuing series of seizures without a period of recovery between episodes ▪ Dementia Progressice deterioration and continuing decline of memory and other cognitive changes 60 % to 80 % of Alzheimer are dementia- Vascular dementia is the most common cause No cure Cause is unknown Dementia-causing illness: - Alcoholism

- Alcoholism

- Intracranial tumor

- Normal-pressure hydrocephalus

- Parkinson disease

- Lewy body disease

Spinal Cord Injuries- major mechanisms of injury? A problem of the young Male 3-4x risk – weekends/summer months Motor vehicle crashes- highest number of sci 2) violent gun shot wounds, falls, recreational accident The major Mechanisms of injury are hyperflexion, hyperextension and compression

Flexion injury with tearing of the posterior ligaments and dislocation is the most unstable injury and is aften associated with severe neurologic deficits Hyperextension injury is the most common S/S complete loss of function below the level of injury , Spinal shock (a few hrs) Flaccid paralysis of all skeletal muscles. Loss of all spinal reflexes, loss of pain, proprioception and other sensations, bowel and bladder dysfunction with paralytic ileus, loss of thermoregulation. Bradycardia, hypotension ▪ How to treat Spinal Cord Injuries Stabilization of the spinal vertebra (to prevent further trauma to spinal cord) Sugery – internal fixation or external fixation and bracing Surgery within 24 hrs if cord compression Use od high-dose methylprednisolone (1st^8 hrs) (controversial method) Removing or alleviating the painful stimuli Use od adrenergic receptor-blocking medication to manage hypertensive crisis Prevent respiratory and urinary tract infections Skin pressure sores Septicemia and fecal impaction ▪ Hypoventilation build up what? Hypoventilation causes build up of acid (acidosis) and too little oxygen in the blood. Hypoventilation occurs when delivery of air to the alveoli is insufficient to meet the need to provide O2 and remove CO2.

- Decrease rate and depth of respiration

- Results in increased PaCO2 ≥45 mm Hg

- Hypoxemia – increased alveolar CO

▪ Causes: drugs (morphines, barbiturates) , obesity (Pickwickian syndrome, myasthenia gravis, obstructive sleep apnea, chest wall damage. ▪ Normal ABG’s- Only must know normal values pH 7.35-7. PaCO 2 35-45 mm Hg PaO 2 80-100% HCO 3 22-26 mEq/L SaO 2 95-100% ▪ Acute Respiratory Failure- the goal of treatment Maintaining ventilatory support by maintaining airway patency and ensuring adequate alveolar is the primary goal of therapy. Mechanical ventilation

Virchow (1800 Pathologist) 3 Factors that predisposed patient to thrombus formation an increase of PE (Pulmonary Embolism)

- Venous Stasis (sluggish blood flow

- Hypercoagulability

- Damage to the venous wall (intimal injury)

Box 21. Fa c t o r s P r e d i s p o s i n g t o P u l m o n a r y E m b o l i s m o f Vi r c h o w ' s Tr i a d Venous Stasis

  • Extended bed rest (delayed venous removal of activated clotting factors)
  • Postoperative state
  • Immobility (activated clotting factors)
  • Vascular disorders (thrombophlebitis of lower extremities and pelvic area)
  • Congestive heart failure (venous backflow/stasis)
  • Cardiac dysrhythmias (atrial fibrillation)
  • Dehydration
  • Prolonged air travel
  • Obesity Hypercoagulability
  • Oral contraceptives (estrogen therapy), hormone replacement therapy
  • Pregnancy, early puerperium
  • Polycythemia^ (chronic^ high^ altitude;^ chronic^ pulmonary^ disease^ with^ decreased^ PaO 2 and^ increased PaCO 2 )
  • Malignant pathologic processes, visceral cancer
  • Cigarette smoking
  • Inherited resistance to activated protein C
  • Deficiency of protein S
  • Deficiency of antithrombin III
  • Prothrombin gene mutation
  • Presence of antiphospholipid antibodies (lupus), anticoagulant and anticardiolipin antibodies Damage to Vessel Wall (Intimal Injury)
  • Blunt trauma
  • Penetrating wounds
  • Bone fractures with soft tissue injury
  • Surgical procedures (hip, pelvic, abdominal, cardiovascular)
  • Obstetric manipulations during labor and delivery
  • Burns
  • Central venous catheter

▪ Embolisms the different types ▪ 7 Types of embolisms: ▪ -Thrombotic ▪ -Fat ▪ -Amniotic Fluid ▪ -Air ▪ -Tumor ▪ Foreign material ▪ Septic ▪ Parasite