Patho final Exam concentrated subjects

Hypernatremia

excessive sodim levels in the blood and extracellular fluids

* greater than 145

Causes of hypernatremia

ingestion of large amounts of sodium without proportionate water intake or a loss of water from the body that is faster than the loss of sodium

* Insufficient ADH (large volume of dilute urine)
* Loss of thirst mechanism
* Watery diarrhea
* Prolonged periods of rapid respiration

Effects of hypernatremia

manifests from a fluid shift out of the cells owing to increased osmotic pressure of interstitial or extracellular fluid

* weakness, agitation
* firm subcutaneous tissue
* increased thirst with dry, rough membranes

Hyponatremia

Low sodium levels in the extracellular fluids

* less than 135

Causes of Hyponatremia

* losses from excessive sweating, vomiting and diarrhea
* Uses of certain diuretic drugs combined with low-salt diets
* Hormonal balances: insufficient aldosterone, adrenal insufficiency, excess ADH secretion
* Early chronic renal failure
* Excessive water intake

Effects of hyponatremia

* Impaired nerve conduction and result in fluid imbalances in the compartments: fatigue, muscle cramps, abdominal discomfort or cramps with nausea and vomiting
* Decreased osmotic pressure in the extracellular compartment: hypovolemia, decreased blood pressure

Hyperkalemia

Excessive potassium levels in the extracellular fluids

* greater than 5

Causes of hyperkalemia

* Renal failure
* Deficit of aldosterone
* Use of “potassium sparing” diuretic drugs: prevent potassium from being excreted in a adequate amounts
* Leakage of intracellular potassium into the extracellular fluids
* Displacement of potassium from cells by prolonged or severe acidosis

Effects of hyperkalemia

* Cardiac dysrhythmias that could progress to cardiac arrest
* Muscle weakness; could progress to paralysis
* Fatigue, nausea
* Parethesias: fingers, nose, face
* Oliguria

Hypokalemia

insufficient potassium levels in the extracellular fluids

* less than 3.5

Causes of hypokalemia

* Diuresis associated with certain diuretic drugs
* Presence of excessive aldosterone or glucocorticoids
* Decreased dietary intake
* Treatment of diabetic ketoacidosis with insulin

Effects of hypokalemia

* Cardiac dysrhythmias
* Impaired neuromuscular function and muscles less responsive to stimuli: fatigue and muscle weakness in the legs; twitch, leg cramps
* Paresthesia: abnormal touch sensations such as “pins and needles”
* Anorexia, nausea
* Slow shallow respirations

Acidosis

excess hydrogen ions; decrease in serum pH

Respiratory acidosis

increase in carbon dioxide levels due to respiratory problems

Causes of respiratory acidosis

* Acute respiratory problems such as Pneumonia, chest injuries, use of opiates, airway obstruction (aspiration or asthma)
* COPD: chronic respiratory acidosis is common
* Decompensated respiratory acidosis: severe impairment; when a chronic problem develops an additional infection

Metabolic acidosis

a decrease in serum bicarbonate

Causes of metabolic acidosis

* Shock
* Excessive loss of bicarbonate: diarrhea, loss of bicarbonate in intestinal secretions
* Increased utilization of serum bicarbonate to buffer increased acids
* Renal disease or failure: decreased secretion of acids and decreased production of bicarbonate

Acidosis Effects

impaired nervous function- headache, lethargy, weakness, confusion, coma and death

Acidosis Compensation

deep rapid breathing secretion of urine with a low pH

Alkalosis

deficit of hydrogen ions, increase in serum pH

Respiratory alkalosis

decrease in carbon levels due to respiratory problems

Causes of respiratory alkalosis

Hyperventilation: anxiety, aspirin overdose

Metabolic alkalosis

increase in serum bicarbonate; loss of hydrogen ions through the kidneys or gastrointestinal tract

Causes of metabolic alkalosis

* Vomiting (early stage)
* Excessive antacid intake

Effects of alkalosis

* Irritability of the nervous system: muscle twitching, restlessness, tingling, numbness of finders
* Tetany, seizures, coma

Compensation of alkalosis

slow shallow respirations

ADH

Controls the amount of fluid leaving the body in urine; promotes reabsorption of water into the blood from the kidney tubules

Causes of Pain

* Inflammation
* infection
* ischemia
* tissue necrosis
* stretching of tissue
* stretching of tendons
* ligament
* joint capsule
* chemicals
* burns
* muscle spasm

Gate open

pain stimulus transmitted

Gate closed

Pain stimulus blocked

Ways gates can close

1. sensory stimuli move along competing pathways
2. brain produces outgoing transmissions through reticular system
3. brain release opiate-like chemicals: endorphins block substances at the synapse, natural opiate receptors are through brain

First line of defense:

nonspecific or general mechanism such as skin or mucous membrane

* blocks the entry of bacteria

Second line of defense

innate immune system mechanism

* non-specific process of phagocytosis, inflammation, interferons

Third line of defense

specific mechanism in the body: stimulate the production of antibodies, synthesized t-lymphocytes

Leukotrienes

Group of lipids derived from mast cells and basophils

* cause contraction of bronchiolar smooth muscle and have a role in development of inflammation
* causes coughing

Acute inflammation

self-limiting

Chronic inflammation

persists for week to months

Local effects of inflammation

* erythema and warming
* edema
* pain
* loss of function
* exudate

Systemic effects of inflammation

* fever
* leukocytosis
* elevated values (c-reactive proteins, ESR, cell enzymes
* malaise fatigue
* discomfort

Bacteria

prokaryotic, no nuclear membrane, function metabolically, divide by binary fission, do not require living tissue to survive

* Major groups: cocci (spheres), bacilli (rod-shapes), spirochete (coiled/wavy lines), strepto (chains), staph (clusters)

Spores

a latent form of the bacterium with a coating that is highly resistant to heat and other adverse conditions

* can survive long periods in spore state and remain latent in the body until more favorable conditions

Prions

protein like agents that are transmitted by consumption of contaminated tissues

* infectious agent of Cruetzfeldt-Jakob disease

Cellulitis Patho

infection of the dermis and subcutaneous tissues arising from a secondary injury (boils or ulcers)

* usually from Strep Aures

Cellulitis manifestations

* reddened area
* edematous
* pain
* red streaks running along the lymph vessels proximal to the infected area may develop

Hypoxia

severe reduced oxygen to tissues

IgG

most common in blood

* this is because it is the first antigen produced when they body starts to fight off an infection

IgM

first to increase in immune response

* activates complement
* involved in ABO incompatibility reactions

T cells

cell mediated immunity; WBC

* mature in thymus

B cells

Hemoral immunity

* mature in bone marrow
* activated cells becomes and antibody producing plasma cell becomes and antibody-producing plasma cell or a b memory cell

Memory cells

Remember antigen and quickly stimulate immune response on reexposure

Leukocytosis

elevated WBC

* associated with inflammation or infection

Leukopenia

decreased levels of WBC

* associated with viral infections, radiation, chemotherapy

Hematocrit

percent by volume of cellular elements in blood

Reticulocyte count

assessment of bone marrow function

* RBC maturation and count
* determines if red bone marrow makes enough RBC at appropriate time

Iron-deficiency anemia

insufficient iron impairs hemoglobin synthesis; microcytic (small cells) and hypochromic (less color) RBC, result of low hemoglobin concentration in cells

* Etiology: dietary intake, duodenal absorption, sever liver disease, infections, and cancer

Pernicious Anemia

lack of absorption of vitamin B12 because of lack of intrinsic factor secreted by gastric mucosa

* most common is malabsorption (gastrectomy), dietary insufficiency is rare

Pernicious Anemia manifestations

* tongue enlarged, red, sore, and shiny (because of lack of bloodflow)
* digestive discomfort
* Paresthesia (tingling or burning)
* ataxia (loss of coordination)

Aplastic anemia

impairment or failure of bone marrow

* often idiopathic, myelotoxins (radiation, industrial chemicals, drugs), viruses (hep C), genetic abnormalities (myelodysplastic syndrome, Fanconi’s anemia); chemotherapy!!!

Aplastic anemia manifestations

* anemia
* leukopenia
* thrombocytopenia
* petechiae: flat, red, pinpoint hemorrhages on the skin

Sickle Cell Anemia

inherited characteristics leads to the abnormal hemoglobin S (Hbs); one amino acid in the pair of beta globin chains has been framed to normal glutamic acid to valine;

* causes hemolysis and obstruction of small vessels
* shape causes clogged
* any stress on the body can be a factor
* genetic condition, occurs in homozygous recessive, autosomal, incomplete dominance
* blood test to detect gene

Hemophilia

type A is deficit or abnormality of clotting factor VIII and it the most common inherited disorder, transmitted as an X-linked recessive trait

* type b is factor XI
* type C is a milder form
* Manifestations: prolonged or severe hemorrhage; persistent oozing blood after minor injuries; spontaneous hemorrhage of joints; hematuria

Conduction Pathway

* Sinoatrial node (SA): pace maker, sinus rhythem
* Atrioaventriclar node (AV node): located on in floor of the right atrium
*   AV bundle (bundle of His): right and left branches
* Purkinje fibers: terminal fibers

Electrocardiogram

* P wave: depolarization of atria
* QRS wave: Depolarization of ventricles
* T wave: repolarization of ventricles

Angina pectoris

occurs when there is a deficit of oxygen to the heart muscle

* oxygen or blood supply impairment; when the heart is working harder than usual and needs more oxygen
* types: classic or extertional, variant, unstable

Variant Angina

vasospasm occurs at rest

Unstable

prolonged pain at rest

* may precede MI
* results in a break down of atheroma

Myocardial Infarction (MI)

occurs when coronary artery is totally obstructed leading to prolonged ischemia or infarction of the heart wall

Myocardial Infarction Causes

atherosclerosis with attached thrombus

* thrombus builds up to obstruct the artery, vasospasm (small percentage) may occur in the presence of atheroma leading to total obstruction, part of thrombus breaks away forming and embolus that is then lodged into a smaller branch

MI Complications

* Sudden death
* Cardiogenic shock
* Congestive heart failure
* Rupture of necrotic heart tissue/cardiac tamponade
* Thromboembolism causing cerebrovascular accident (CVA; with left ventricular MI)

MI treatment

* Reduce cardiac demand
* Oxygen therapy
* Analgesics
* Anticoagulants
* Thrombolytic agents may be use
* Tissue plasminogen activator

Congestive Heart Failure

occurs when heart is unable to pump sufficient blood to meet the metabolic needs of another conduction

* usually occurs as a complication of another condition, infarction, valve defect
* Left and right sided

Left sided CHF causes

* infarction of left ventricle
* aortic valve stenosis
* hypertension
* hyperthyroidism

Left Sided CHF Basic Effects

* decreased cardiac output
* pulmonary congestion

Left and right sided CHF forward effects

* fatigue
* weakness
* dyspnea
* exercise intolerance
* cold intolerance

Left and right sided CHF Compensations

* tachycardia
* pallor
* secondary polycythemia
* daytime oliguria

Left Sides CHF Backup effects

* orthopnea
* cough producing white or pink tinged phlegm
* shortness of breath
* paroxysmal nocturnal dyspnea
* hemoptysis
* rales

Right sided CHF Causes

* infarction of right ventricle
* pulmonary valve stenosis
* pulmonary disease

Right sided CHF back up effects

* Dependent edema in feet
* hepatomegaly and splenomegaly
* ascites
* distended neck veins
* headache
* flushed face

Hypovolemic shock

loss of blood or plasma in blood vessels

* Causes: hemorrhage, burns, dehydration, peritonitis, pancreatitis

Cardiogenic shock

decrease pumping capability of the heart

* Causes: Myocardial infarction of left ventricle, cardiac arrhythmia, pulmonary embolus, cardio tamponade

Vasogenic (neurogenic or distributive)

vasodilation owing to loss of sympathetic and vasomotor tone

* Causes: pain and fear, spinal cord injury, hypoglycemia

Anaphylactic shock

systemic vasodilation and increased permeability owing to severe allergic reaction

* Causes: insect stings, drugs, nuts, shellfish

Septic Shock

vasodilation owing to severe infection, often with gram neg bacteria

* Causes: virulent microorganisms (gram neg bact), multiple infections

Early shock manifestations

* anxiety
* tachycardia
* pallor
* light-headedness
* syncope
* sweating
* oliguria

Hypertension Development

* Systemic vasoconstriction
* decreased blood flow to kidneys 
* Increased renin secretion which can lead to


1.   Systemic vasocontraction → increased peripheral resistance
2. Aldosterone secretion → increased blood volume

* Increased blood pressure

Effects of hypertension

o   Damage to renal blood vessels (kidneys)

o   Increased work for the heart causing left sided CHF

o   Damage to cerebral arteries causing stroke

o   Damage to arterial walls leading to atherosclerosis

o   Damage to retinal blood vessels causing blindness (eyes)

Tidal volume

amount of air entering lungs with each normal breath

Residual volume

amount of air remaining in the lungs after forced expiration

Inspiratory Reserve

maximal amount of air that can be inhaled in excess of normal quiet inspiration

Expiratory reserve

maximal volume of air expired following a passive expiration

Vital capacity

maximal volume of air expired following a passive expiration

Total lung capacity

total volume of air in the lungs after maximal inspiration

COPD

Group of chronic respiratory disorders

* Causes irreversible and progressive damage to lungs; Debilitating conditions that may affect individual’s ability to work; May lead to the development of cor pulmonale; Respiratory failure may occur

Emphysema

destruction of alveolar walls and septae

* leads to large permanently inflated alveolar air spaces
* loss of elasticity
* little sputum, some infections and late Cor pulmonale
* Break down of alveolar wall results in: loss of surface area for gas exchange, loss of pulmonary capillaries
* Etiology: smoking, genetics

Emphysema Manifestations

* dyspnea
* hyperventilation with prolonged expiratory phase
* clubbed fingers
* barrel chest
* pursed lip breathing

Chronic bronchitis

increased mucous glands and secretion, inflammation, obstruction, infection, chronic coughing for 3 months or longer in 2 years

* large amounts of sputum
* Etiology: smoking, air pollution
* cough dyspnea: early constant cough, dyspnea

Chronic Bronchitis manifestations

* constant productive cough
* tachypnea
* shortness of breath
* blue bloater
* hyperventilation
* cyanosis in lips, mucous membranes, nail beds

Pulmonary Edema

fluid collecting in the alveoli and interstitial area; reduces the amount of oxygen diffusing into the blood and interferes with lung expansion

* May develop when: inflammation is present in the lungs, increasing capillary permeability, plasma protein levels are low, decreasing plasma osmotic pressure; pulmonary hypertension develops

Pulmonary Edema causes

* left sided heart failure
* hypoproteinemia (due to kidney or liver disease)
* inhalation of toxic gases
* association with tumors
* blocked lymphatic drainage due to fibrosis or tumors
* obstructive sleep apnea

Pulmonary edema manifestations

* cough
* orthopnea
* rales (in mild cases)
* frothy blood tinged-sputum