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 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 4th 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
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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 4th^ 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

Hepatic encephalopathy is usually precipitated by certain well-defined clinical developments, including hypokalemia, hyponatremia, alkalosis, hypoxia, hypercarbia, infection, use of sedatives, GI hemorrhage, protein meal gorging, renal failure, and constipation. In some patients, progressive liver failure leads to chronic encephalopathy without other exacerbating factors. Hepatic encephalopathy is graded 1 to 4:  Grade 1: Confusion, subtle behavioral changes, no flap  Grade 2: Drowsy, clear behavioral changes, flap present  Grade 3: Stuporous but can follow commands, marked confusion, slurred speech, flap present  Grade 4: Coma, no flap  Gastroesophageal Varices Management

  • Initial treatment: Fluid resuscitation to stop bleeding
  • Large bore intravenous lines are placed
  • Admin of parenteral vitamin K and plasma, platelet infusion if thrombocytopenia is present
  • Octreotide acetate (synthetic analog) no more vasopressin 3-5 days
  • Metoclopramide and B blockers
  • Esophagogastroduodenoscopy EGD to determine site of bleeding  Difference between Diverticulosis and Diverticulitis Diverticulosis (diverticular disease) presence of diverticula in the colon. Diverticula are acquired herniations of the mucosa and submucosa through the muscular coat of the colon Diverticulosis The presence of one or more diverticula vs diverticulitis inflammation of one or more diverticula  Kidney Disease- Assessment-CVA Pain associated with intrarenal disorders are assessed by palpating or light percussion over the costovertebral angle (CVA) posteriorly and is recorded as CVA tenderness. Pain is transmitted to the spinal cord between T10 and L  Kidney Cancer signs and symptoms Benign renal neoplasm: S/S Hematuria and flank pain Some may be asymptomatic until large Renal cell carcinoma: Metastatic disease Risk factors: smoking, obesity and hypertension S/S CVA tenderness, hematuria, palpable mass  Dialysis- Benefits and Risks  Filter blood and rid the waist Dialysis is the only therapeutic option for those with ESRD unable to obtain transplant Each treatment of dialysis remove about 2/3 of the total body urea content Dialysis maintain volume status Prevent and treat acid-base and electrolyte disturbances Prevent and treat uremia Support nutritional needs. Prevent and treat infection Orevent 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

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.

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 Syndrome Adrenocortical 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  Mechanisms of injury

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

- 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 The major Mechanisms of injury are hyperflexion, hyperextension and compression

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. F a 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 V i 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 

Embolism Typ e Cause 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  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)

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 PaO (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

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

Over 15 – 25% Chest tube placed with water seal and suction 100 % oxygen Chemical pleurodesis Thoracotomy

 Pneumonia

Pneumonia (breath) An inflammatory reaction in the alveoli and interstitium of the lung usually caused by an infectious agent Pneumonia can result from 3 sources

- Aspiration of oropharyngeal secretions of bacterial flora and or gastric

contents (20-35 % of all pneumonia)

- Inhalation of contaminants (virus, mycoplasma)

- Contamination from the systemic circulation

Classifications of Pneumonia : Community acquired/hospital acquired 15-20 % with pneumonia requires hospitalization Pneumonia classified: bacterial Atypical Viral Pneumonia : Gram positive Gram negative Gram positive: Staphylococcus and streptococcus Gram negative: E coli, Hearmophilus influenza, kleb, Risk: Elderly , diminisged gag reflex, seriously ill., hospiralized, hypoxix immunocompromised

 TB- transmission

Transmission: It is a airbone disease

- inhalation of small droplets containing bacteria

TB baccillus

- Droplets expelled with cough, sneeze, or talking

Bacteria Mycobacterium tuberculosis – acid fast aerobic bacillus  Most common sites are the lungs and the lymph nodes 

 Sources of Electrolyte Stores

Every fluid compartment contains electrolytes- Electrolytes compositions differs in each compartments. The concentration of K, Mg, Ca is higher inside cells than fluids outsise of cells. Total calcim ions content concentration is higher inside cells, intracellular calcium is bound to other molecules. The concentration of active ionized Ca ions is higher in the extracellular fluids. The cells and bones are called electrolyte pools as they serve as important reservoir of Ca, K, Mg. Distribution of electrolytes between the extracellular fluid / the electrolyte polls is influenced by hormones (epinephrine – K ions) (Isulin – K and Ph ions) and PTH (calcium ions) PG 531 Electrolyte Distribution

 Anemia Anemia is a deficit of red cell  _- Low oxygen-carrying capacity leads to hypoxia.  Opposite of anemia: polycythemia  Excess of red cells  Increases blood viscosity and volume  Relative anemia—normal total red cell mass with disturbances in regulation of plasma volume  Absolute anemia—actual decrease in numbers of red cells  Decreased production  Increased destruction  Hormone that Kidney’s secrete  • The kidney secretes two important endocrine hormones: erythropoietin, a growth factor for red blood cells (RBCs), and active vitamin D, a necessary cofactor for calcium absorption from the intestine.  • In chronic kidney disease, impaired production of these hormones results in anemia and osteodystrophy.  Definition of Polycythemia Red cells are present in excess increasing blood viscosity which turns cause hypertension. 3 Types of polycythemia: - Polycythemia vera- neoplastic transform bones marrow

- Secondary Polycythemia – chrnic hypoxemia (over production of

erythropoietin)

- Relative polycythemia

 Thrombocytopenia is caused by

- Decreased platelet production

o Folate/b12 deficiency o Radiation therapy o Chemotherapy o Drugs (ETOH, Thiazides, phenytoin) o Aplastic anemia o Cancer in bone narrow

- Decreased platelet survival

o Drugs (Thiazides, digoxin, heparin, furosemide, certain antibiotics o Mechanical prosthetic heart valves o Viral and bacterial infections o Circulating immune complexes o Increased destruction in the spleen o Disseminated intravascular coagulation

- Splenic Sequestration (pooling)

o Splenomegaly o Hypothermia

- Platelet dilution

o Massive transfusion with blood stored more than 24 hrs Thronmocytopenia is caused by Generalized bleeding  Disseminated Intravascular Coagulation (DIC)- What is it? And How to treat it? Disseminated intravascular coagulation (DIC) is a acquired hemorrhagic syndrome in which both clotting and bleeding occur simultaneously.

Weight loss Malaise -Cerical nodes -lymp nodes enlargements above diaphragm Iguinal nodes -Disease spread from site of origin to other lymph nodes (spleen and bone narrow) Prognosis and treatment Ann Arbor staging also used for NHL Stages of HD A: Absence of clinical symptoms B: Symptoms present at time of staging (Loss of 10 % or more body weight, Unexplained fever, night sweats) CS: Hx. PA, noninvasive procedures (computed tomography (CT scan) PS: Invasive procedure such as laparotomy and tissue biopsy (Non-Hodgkin) B-call, T-call and NK-Cell lymphoma  Hypertension- Modifiable and Non-Modifiable Factors Most common primary diagnosis in the US> Heart disease, kidney disease, peripheral vascular disease and stroke. Responsible for 7.6 mil (worlwide) Prehypertension – range between normal blood pressure (120/80) to stage 1 hyper

- Stage that we initiate efforts to prevent or deter progression of disease

Primary hypertension- essential hypertension – Silent killer - Sys BP

≥ 140 mmhg Dias BP < 90 mmHg

Most common form of hypertension Rare prior to age 10- Major risk for cardiovascular disease Complication: End-organ damage, renal failure, stroke, heart disease, increase myocardial work in HF, Treatment: Lifestyle modifications, wgt loss, exercise, DASH diet, alcohol moderation. Decrease sodium intake. Drug therapy for heart rare, SVR and stroke Modifiable: - dietary factors, sedentary lifestyle, obesity/weight gain, metabolic syndrome. Elevated blood glucose levels/Diabetes, elevated cholesterol, alcohol and smoking Non-modifiable: Family hx, age, ethinicity/genetics (maternal smoking, pregnancy induced hypertension, low birth rate)Hypertension- Organs effected o Renal (Parenchymal and vascular) o Cardiovascular o Tumor o Endocrine (Hyperthyroidism, cushing disease, congenital adrenal hyperplasia, primary hyperaldosteronism) o Neurologic (Guillain-Barre Syndrome, Increased intracranial pressure) o Other (Systemic arteritis. Sleep apnea)  Hypertension is the most common primary diagnosis in U.S  32 % of 80 mil adults in U.S has High Blood Pressure  Higher in Non-hispanic black adults (44.9 %)  Hypertension is the most common Risk factor for cardiovascular worldwide

 Normal Range fore blood pressure is 120 mmHg systolic – 80 mmHg diastolic – 18 and older  Prehypertension : range between normal BP to Stage 1 Hypertension  Stage 1 Hypertension : Sys 140 mmHg or dias 90 mmHg  Primary Hypertension (essential hypertension)  No clear cause so idiopathic disorder  Different than secondary hypertension where blood pressure elevation is cause  Primary hypertension most common 90-95 %  Systolic blood pressure is the major risk for subsequent cardiovascular disease  Hypertension- Management

- Lifestyles modifications

- Drug therapy (heart rate, stroke, Systemic vascular resistance)

Coronary Artery Disease CHD (Ischemic Heart disease) CA. Insufficient delivery of oxygenated blood to the myocardium (Ischmea) because of the atherosclerotic coronary arteries. CHD cause 1 in 6 death in UD. _ (dysrhythmias, sudden cardiac arrest, heart failure) Ethiology: Atherosclerosis of coronary arteries is the source od nearly all SHD Risk factors: Family Hx, Abd lipid levels, smoking, hypertension, diabetes, obesity )Definition of Atherosclerotic Plaques They are plaques that are from injury to the coronary artery endothelium and they are filled with large lipid core, fragiles and prone to ruptures.  Myocardial Ischemia- What is it It is when blood flow to the heart muscle (myocardium) is obstructed by a partial or complete blockage of a coronary artery by a buildup of plaques (artherosclerosis) If plaques ruptured, you can have a heart attack (myocardial infarction)  Acute Coronary Syndrome Risk : Smoking, Fam Hx, Obesity, Lifestyle sedentaty, diabetes, poor diets, lipids Up S/S ; MI Chest pain (more severe than typical angina) (patient might say elephant sitting on chest) Chest pain that may radiate to the arm shoulder , jaw and back N/V Diaphoresis (sweating) SOB (dyspnea) Etiology: Plaqu rupture with thrombus development Unstable Angina – Occlusion is partial With MI- Occlusion is complete Treatment: Decrease myocardial oxygen demand – increase myocardial oxygen supply Monitor and manage complications Diagnosis : EKG and Biomakers  Definition of Unstable Angina Pectoris  Chest pain associated with intermittent myocardial ischmia (Burning, crushing, squeezing, choking, or referred pain)

- Result from inefficient cardiac pumpin (resultant pulmonary

congestion and SOB)