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Spring Completed 2023
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-
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?
Spring Completed 2023
Hepatic encephalopathy is a decline in brain function due to severe liver disease
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RISKS
Electrolytes imbalance (potassium and sodium) -need to check hyper or hypo
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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 Ac ute Ki dney Inj ury
Prerenal
- • Absolute decrease in circulating volume
o • Hemorrhage
o • Dehydration
o • Burns
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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
o • Acute glomerulonephritis
o • Acute allergic interstitial nephritis
o • Acute pyelonephritis
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.
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▪ What is the Glomerelus?
▪ It is a segment of nephron that filters fluid from blood into Bowman capsule,
prevents passage of blood cells and proteins.
▪ What is Glomerulonephritis?
▪ An assortment of immune-mediated conditions that produce inflammation of the glomeruli.
▪ Diabetes Type I and Type II
Type 1: Destruction of the B cells of the pancreas results in absolute insulin
deficiency 5-20 yrs
Chromosone 6
Type 2: Most common form of DM – Insulin resistance and B cells dysfunction lead to a
resistance lack of insulin
Risk factor: Female sex, obesity, and sedentary lifestyle
Risk factor: non Caucasian, elderly
▪ Poly’s of Diabetes
▪ 3 P : Polyuria, Polyphagia, Polydipsia
▪ Cushing’s Syndrome characterized by
Cushing
Adrenocortical Syndrome
Insufficiency
Truncal
obesity
Moon face
Dorsocervical
fat pad
Hirsutism
Muscle
wasting
Striae
Petechiae
Glucose
intoleranc
e
Hypertension
Hypokalemia
Weakness
Hypotension
Hypoglycemia
Hyperpigmentatio
n
(Addison
disease)
Hyperkalemia
Weight loss
▪ Traumatic Brain Injury
➢ Traumatic brain injury (TBI) refers to injuries of brain tissues sustained as a
consequence of trauma
➢ 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
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➢ 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
Transient ischemic attack (TIA) – Episodes of stroke s/s with a duration of less than 24 hr and less
than1hr (30% pt with stroke have prior
TIA) Ischemic stroke- Sudden occlusion of cerebral artery secondary to
thrombus formation/embolization
- Thrombotic strokes: atherosclerosis and hypercoagulable states
- Embolic strokes: cardiac sources
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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
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- Huntington disease
- Multiple sclerosis MS
- Bocine Spongiform encephalopathy (Mad
Cow) Delerium and depression in elederly different than dementia
Delirium in global mental dysfunction – Acute Confusional state
Primary risk factor: age and family
Others: Head trauma, diabetes, depression, stroke, hypertension diabetes
Signs and Symptoms memory lost, anxiety and agitation, diffulty in judgement, problem
solving and communication. Assistance needed for ADL. Difficulty eating and swallowing.
Weight loss
▪ Parkinson disease
Disorder of mobility - 1 million americans affected. 60,000 cases each year
4 % are younger than 50
Y/O idiopatic or acquired
Common causes: Infection, intoxication, and trauma
Drug Toxicity: Phenotiazine class: (Chlorpromazine, prochlorperazine, Thioridazine) and
Butyrophenone(haloperidol)
Parkinson disease results from degeneration of the pigmented dopaminergic neurons found
in the subtantia nigra and to a lesser extent neurons elsewhere in the brain.
Lewy bodies are cytoplasmic inclusions are found in the surviving neurons.
▪ GERD signs and symptoms
Heartburn
Chest pain
Regurgitation
Epigastric pain
Dry cough
Hoarseness in the morning
Esapheogeal strictures with
Gerd
▪ Multiple Sclerosis- Structures effected by the demyelination?
Chronic demyelinating disease of the CNS – sign disability in young adults
Autoimmune disorder that results in inflammation and scarring of the myelin sheaths
covering nerves.
Age onset (20-50 yr)
2 -3x more common in women vs men
In MS, the demyelination of nerves can happen anwhere in the CNS. Structures most
frequently affected are the optic nerves, the oculomotor nerves, the corticospinal,
cerebellar, and posterior column system.
Myelin facilitates nerve conduction. So the inflammation with MS slow or interrupt the
conduction of nerve impulses.
▪ 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
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The major Mechanisms of injury are hyperflexion, hyperextension and compression
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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
Final REVISED Final Exam Study Guide Patho
Spring Completed 2023
▪ Asthma- definition
Asthma is complex lung disease and associated with the release of inflammatory
chemicals from mast cells in the airways.
Asthma is a lung disease characterized by:
- airway obstruction that is reversible (to some patients)
- airway inflammation
- increased airway reactivity to a variety of stimuli
Mast cell release are IgE (immunoglobin E) mediated for both extrinsic and intrinsic asthma.
Extrinsic Asthma: Allergies, family hx of the disease. Positive reaction to environmental
triggers.
Intrinsic Asthma: Respiratory Tract infections and psychological factors(harder to treat)
Embolism Typ
Cause
e
Thrombotic Blood clots develop in venous system, predominantly in thighs and legs
Fat Globules of fat secondary to fractures of pelvis or long bones
Amniotic fluid Collections of fluid, hair, or other debris related to complicated labor,
especially in olde multiparous women
Air Venous access through IV catheters
Tumor Fragments from malignant tissue
Foreign
material
Foreign bodies (bullets, sutures, catheter tips, orally prepared medications
injected IV)
Septic Infected tissue or related substances (fungal/bacterial)
Parasitic Parasites present in lung vasculature
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Pathogenesis: Chronic inflammation and swelling of the bronchial mucosa resulting in scarring,
increased fibrosis of the mucous membrane, hyperplasia of bronchial mucous glands and
globet cells, hypertrophy of bronchial wall thickness which cause (potentiates) obstruction to
airways.
Neutrophil activity cause inflammation.
Interleukin-8 levels are elevated. CD8 T-lymphocyte levels are elevated.
Two bacteria is involved with chronic bronchitis: H. influenza and S.Pneumoniae
The chronic bronchitis patient appear as the blue bloater: Oxygen desaturation (cyanosis) and
edmea associated with right-sided heart failure.
S/S of Chronic Bronchitis:
- Overweight (1:2 male to female ratio)
- 30s and 40s
- SOB (shortness of breath) on exertion
- Excessive amounts of sputum (mixture of saliva and mucus)
most severe in the am
- Chronic cough
- Excess of body fluids( edema, pypervolemia)
- Hx of smoking
- Complaints of chills
- Malaise
- Muscle aches
- Fatigue
- Loss of libido
- Insomnia
End-stage of Chronic Bronchitis, Patient has
- Right-side heart failure
- Distended neck veins
- Right ventricular heave
- Right ventricular gallop
- Peripheral edema
- Hypoxia- pulmonary hypertension
- Cyanosis
Diagnosis: Chest radiography, pulmonary functions tests, Elevated PaCO2 and decreased
PaO2 (below 65 mmhg)
Severe Chronic Bronchitis: Physical Exam: Scattered crackles, rhonchi, wheezes, jugular vein
distension, clubbing, pedal and ankle edema
Treatment: Because Bronchitis and Emphysema has similar
therapy 1- Block the progression of the disease
2- Return the patient to optimal respiratory function
3- Return the patient to usual activities of daily
living
Inhaled B-2 agonists
Inhaled anticholinergic brichodilatoes
Cough suppressants
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Antimicrobial agents for infection
Inhaled or oral cortisosteroids for acute exacerbations
Low-dose of Oxygen therapy for patient with Pao2 less than 55 mmhg
Mechanical ventilation
Home oxygen
therapy Smoking
cessation
Emphysema 1
Type A COPD – destructive changes of the alveolar walls and abnormal enlargement of
the distal air sacs.
Causes: smoking, air pollution, occupations (Welding, mining, working with asbestos),
∞-1 antitrypsin deficiency
(1%). Develop over a long
period Person over 50
Cigarette smoking in excess of 70 pack -years
Pathogenesis: Pathologic changes leading to alveolar destruction are associated with the
released of proteolytic enxymes from inflammatory cells such as neutrophils and
macrophages.
How does smoking causes alveolar damages? 2 ways:
- Leads to inflammation in the lung tissue (parenchyma)
- It inactivates ∞-1 antitrypsin which would usually protect the
lunc parenchyma.
S/S of patients with emphysema
- Exertional dyspnea
- Thin person over 55 years
- Increased SOB for past 3+4 yrs
- Increase with women who smoke
- Use of accessory muscles to breathe
- Progressive dyspnea
- Pursed-lip breathing
- Minimal Cough
- Barrel chest -Overinflation – increase lung volume
- Digital clubbing
At RISK: Pneumothorax, chest pain on the affected side, dyspnea
Late: Major symptom is dyspnea on exertion. Pink puffers
Treatment the same as chronic Bronchitis Cessation of smokins
▪ Chronic Obstructive Pulmonary Disease
▪ Acute Respiratory Distress Syndrome (ARDS)
ARDS is characterized by damage to the alveolar-capillary
membrane Mortality rates ranges from 30% To 50 %
Decline in the PaO2 (does not respond to O2 therapy)
The common denominator appears to be increased permeability of the pulmonary
vasculature
