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Advanced Pathophysiology HESI review
Get Quizlet's official HESI A2 - 1 term, 1 practice question, 1 full practice test
Terms in this set (55)
low pH, low HCO3
high pH, high HCO3
low pH, high CO2
high pH, low CO2
metabolic acidosis causes
Primary Cause: Addition of large amounts of fixed acids to body fluids; Contributing Causes: Lactic acidosis (circulatory failure), Ketoacidosis (diabetes, starvation), Phosphates and sulfates (Renal dz), Acid ingestion (salicylates), Secondary to respiratory alkalosis, Adrenal insufficiency
metabolic alkalosis causes
Primary Cause: Retention of base or removal of acid from body fluids; Contributing Causes: Excessive gastric drainage, Vomiting, Potassium depletion (diuretic therapy), Burns, Excessive Sodium Bicarb admin
respiratory acidosis causes
Primary Cause: Hypoventilation (causes hypercapnia); Contributing Causes: COPD, Pulmonary dz, Drugs, Obesity, Mechanical asphyxia, Sleep Apnea
respiratory alkalosis causes
• Primary stimulation of CNS: hyperventilation. Can be due to emotional origin (anxiety, fear, apprehension), CNS infection (encephalitis), or salicylate poisoning.
• Reflex stimulation of CNS. Hypoxia stimulates hyperventilation (heart failure, pneumonia, pulmonary emboli).
Can also be stimulated by fever.
• Mechanical hyperventilation, resulting in "over breathing."
Neuro exams include:
-hand strength, limb strength
-ability to follow commands
-ability to move eyes in equal and uniform fashion
-deep pain stimulus response
-symmetrical and coordinated movement
Acute Bronchitis patho
infection or inflammation of the bronchi. In more than 90% of individuals, this is a self-limiting disorder caused by viruses.
will not have high fevers and will have only scattered coarse wheezes on examination without evidence of pulmonary consolidation.
Chest X-ray examination is usually normal.
Chronic Bronchitis patho sequence
The chronic bronchitis pathophysiologic sequence of events is as follows:
Hypersecretion of bronchial mucus, which leads to
Recurrent respiratory infections, which lead to
Airway inflammation, which leads to
Bronchospasm and irreversible airway obstruction
chronic bronchitis patho
characterized by chronic inflammation with recruitment of neutrophils, macrophages, and lymphocytes to the lung, with progressive damage to airways and the lung parenchyma.
hyperplasia of the mucus-producing goblet cells of the bronchial epithelium occurs, resulting in the production of large amounts of mucus in the airways.
Mucus accumulation facilitates the colonization and growth of bacteria, which further contributes to airway inflammation, bronchospasm, and eventual scarring.
Narrowed airways cause v/q mismatching and expiratory airway obstruction with air trapping, resulting in both hypoxemia and hypercapnia.
CAD risk factors pathological
Gender (men > women before age 55, women > men after age 55)
Diabetes mellitus and insulin resistance
Markers of inflammation
C-reactive protein (CRP)
Chronic kidney disease
Air pollution & ionizing radiation
Coronary artery calcification and carotid artery wall thickness
-Injury to endothelial lining
-LDL penetrates vessel wall
-release enzymes & oxygen radicals that oxidize LDL
-foam cells occur that form fatty streak
-collagen deposits & makes firm plaque
CKD patho - lab values
azotemia - increased serum urea, serum creatinine, & other nitrogenous compounds
elevated creatinine clearance
GFR < 15 mL/min = dialysis
colon cancer risk factors
-Diet: high fat, high red meat, low fruits, low fiber
Colon cancer screening
Begin at 50
FOBT (fecal occult blood test)
Colonoscopy q 10y
-monitoring for recurrence using eval of serum levels of tumor marker carcinoembryonic antigen (CEA)
colorectal cancer manifestations
gradual onset of changes in bowel movements, melena or hematochezia, weight loss, abdominal pain, and bowel obstruction.
characterized by upper extremities flexed at the elbows and held closely to the body and lower extremities that are externally rotated and extended.
occurs when the brainstem is not inhibited by the motor function of the cerebral cortex.
swollen, twisted veins in the esophagus that are especially susceptible to ulceration and hemorrhage
hematemesis with resultant severe blood loss, hypotension, and even death.
risk factors for esophageal varices
Elevated pressure in the portal vein is a risk factor for bleeding EVs.
Red color signs are elevated red areas that are important for predicting the risk of variceal bleeding, and red wale markings, dilated venules oriented longitudinally on the mucosal surface, have been considered to be the sign with the highest risk
Constipation, vomiting, severe coughing, and excessive consumption of alcohol may precipitate rupture of EVs.
Scombroid fish poisoning
Toxicity due to ingestion of contaminated fish in which bacterial substances convert compounds in fish tissue to histamine, more correctly called histamine fish poisoning because affected fish can come from families other than Scombroidei.
MOA: Bacterial histidine decarboxylase converts histidine to histamine (which is not degraded by cooking)
AE: Acute-onset burning sensation of the mouth, flushing of the face, erythema, urticaria, pruritus, headache; may cause anaphylaxis-like presentation
Misc: Caused by consumption of dark-meat fish improperly stored at warm temperature; frequently misdiagnosed as allergy to fish; treat supportively with antihistamines
foodborne illness symptoms
Inflammation of the gastrointestinal tract lining (gastroenteritis)
Two major symptoms distinctive of more severe glomerulonephritis are (1) hematuria with red blood cell casts and (2) proteinuria exceeding 3 g/day to 5 g/day with albumin (macroalbuminuria) as the major protein
Flank or back pain
Decreased urine output
General signs of inflammation: malaise, fatigue, headache, anorexia, and nausea
Blood pressure increase
Acute poststreptococcal glomerulonephritis
Cloudy tea colored urine
Discomfort-headache, ab pain, dysuria
Facial edema in morning
Ab edema in evening
Mild to severe hypertension
Renal-BUN and creatine
ASO titer- positive for the presence of strept antibodies
AHase and ADNase-B
Serum complement (C3)
Chest x ray
Acute poststreptococcal glomerulonephritis patho
-group A streptococcal infection leads to antibodies to form immune complexes that are deposited in the glomerular capillaries.
-Complement, polymorphonucleocytes (neutrophils), and monocytes are activated.
-Inflammatory cytokines and toxic oxygen radicals are also released.
-altered permeability leads to proteinuria & hematuria
-Coagulation system activated and deposition of fibrin leads to scarring
Gout patient teaching
monitor for tophi/renal stones
low purine diet
Low purine diet
Excludes foods such as liver, kidney, sweet breads, brains, heart, anchovies, sardines, meat extracts, gravies, fish roe, herring.
heart failure exacerbation
excessive salt intake due to lack of knowledge of, or failure to comply with, salt restriction;
other miscellaneous noncardiac disorders;
use of inappropriate medications (antiarrhythmic agents, calcium channel blockers, or inappropriate reductions in other CHF medications);
and development of arrhythmias (primarily tachyarrhythmias).
Hashimoto's thyroiditis patho
The vast majority of cases result from thyroid inflammation, primarily autoimmune thyroiditis (Hashimoto disease).
Hashimoto disease is an idiopathic autoimmune disorder in which autoreactive T cytotoxic lymphocytes and autoantibodies attack the gland, causing apoptosis and tissue destruction.
acute pertussis patho
gram negative bacterium Bordetella pertussis that produces mutiple antigenic and biologically active products:
Filamentous hemagglutinin (FHA)
primarily a toxin-mediated disease. The bacteria attach to the cilia of the respiratory epithelial cells, produce toxins that paralyze the cilia, and cause inflammation of the respiratory tract, which interferes with the clearing of pulmonary secretions.
acute chest syndrome in sickle cell disease
ACS in SCD is defined as the presence of fever and/or new respiratory symptoms accompanied by the presence of a new pulmonary infiltrate on chest X-ray.
-mild respiratory illness
-acute respiratory distress syndrome.
-presence of severe hypoxemia is a useful predictor of severity and outcome.
- increased adhesion of sickle red cells to pulmonary microvasculature in the presence of hypoxia.
-pulmonary fat embolism,
Macrocytic (megaloblastic) anemias
unusually large stem cells (megaloblasts) in the bone marrow that mature into larger than normal erythrocytes (macrocytes). This is due to ineffective erythrocyte DNA synthesis caused by inadequate vitamin B12 or folate. These anemias can also be caused by the direct effects that excessive alcohol intake and some drugs have on the bone marrow.
pernicious anemia patho
caused by vitamin B12 deficiency. Chronic atrophic gastritis leads to an inability to produce intrinsic factor (IF), which is essential for the absorption of dietary vitamin B12 from the ileum. Decreased absorption of vitamin B12 causes abnormal erythrocyte DNA synthesis.
Pernicious anemia results in two types of clinical manifestations including those due to:
Anemia (impaired oxygen-carrying capacity)
Fatigue, dyspnea on exertion, pallor, dizziness, and palpitations.
Vitamin B12 deficiency
Paresthesias, muscle weakness, and ataxia (neurologic complications); glossitis (tongue inflammation) and atrophic gastritis may also be present.
Folate deficiency anemia
inadequate dietary folate intake. causes:
diet low in veggies
-same as for generalized anemia -may also include stomatitis
Microcytic anemia patho
altered morphology is due to ineffective erythrocyte formation caused by disorders of iron metabolism, disorders of porphyrin and heme synthesis, or disorders of globin synthesis
microcytic anemia symptoms
Symptoms are those of generalized anemia but can also include brittle and malformed nails (koilonychias), angular stomatitis, glossitis, dysphagia, gastritis, and neurologic symptoms such as numbness, irritability, paresthesias, gait disturbances, headache, confusion, and memory loss. Some individuals will experience pica, which is a craving for non-nutritional substances such as clay and dirt. Iron deficiency anemia in children is associated with a number of serious health problems, the most significant of which is cognitive impairment which may be irreversible.
CHF with reduced EF
heart is unable to generate sufficient cardiac output (CO) to sustain vital tissues. The inadequate CO develops because of problems with one of three primary determinants of stroke volume:
contractility, preload, afterload
systolic HF cycle
- increased peripheral resistance and afterload
-further contributed to decreased contractility
neurohumoral factors of CHF
catecholamines, angiotensin II, aldosterone, arginine vasopressin, and natriuretic peptides (atrial and brain natriuretic peptides) contribute to myocardial remodeling and changes in vascular and renal function that, over time, result in a gradual decline in myocardial contractility that becomes irreversible
inflammatory cytokines of CHF
endothelin, tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) contribute to vasoconstriction and myocardial remodeling. These inflammatory cytokines can have long-term deleterious effects on individuals with heart failure by contributing to muscle wasting, anorexia, malaise, and a gradual decline in myocardial function
insulin resistance and diabetes in CHF
abnormal myocyte metabolism, oxidative changes, and mitochondrial dysfunction as well as damage the heart through the production of advanced glycation end products (RAGE).
metabolic abnormalities of CHF
inadequate supply of oxygen and nutrients to the myocardium. This causes altered function of important genes such as the peroxisome proliferator-activated receptor (PPAR) genes that control fatty acid oxidation. In addition, myocardial starvation and associated high catecholamine levels cause insulin resistance. These changes along with changes in myocyte calcium transport contribute to decreased myocardial contractility and remodeling.
Heart failure with preserved ejection fraction (HFpEF)
diastolic heart failure
-the most common cause of diastolic heart failure is hypertension with hypertrophy of the left ventricular myocardium, but it can also result from constrictive myocardial or pericardial diseases.
Pure HFpEF is characterized by:
An increased left ventricular end-diastolic pressure (LVEDP)
Without a decrease in ejection fraction or increase in preload (left ventricular end-diastolic volume
diastolic heart failure patho
linked to changes in intracellular proteins, changes in calcium transport, and changes in the structure of the myocardium.
- left ventricle becomes stiff (decreased compliance) and cannot relax to take in diastolic filling without increasing pressure.
Most common cause of chronic pancreatitis
reduction in transketolase, PDH, and alpha ketoglutarate dehydrogenase (which all use B1 as a cofactor)
-Portal hypertension (ascites & esophageal varices)
-inability to synthesize proteins (coagulopathy and easy bruising)
-inability to metabolize steroid hormones may contribute to fluid retention (aldosterone and antidiuretic hormone)
and to feminization caused by increased estrogen levels (testicular atrophy, spider angiomata, decreased libido, pectoral alopecia).
chronic venous pressure ulcer
open lesions between knee and ankle that are present with venous disease
Risk factors for development of VLUs include older age, female sex, obesity, trauma, immobility, congenital absence of veins, deep vein thrombosis (DVT), phlebitis, and factor V Leiden mutation.
creatinine and aging
The age-related reduction in creatinine clearance (CrCl) is accompanied by a reduction in the daily urinary creatinine excretion due to reduced muscle mass.
Accordingly, the relationship between serum creatinine (SCr) and CrCl changes. The net effect is near-constancy of SCr while true GFR (and CrCl) declines, and consequently, substantial reductions of GFR occur despite a relatively normal SCr level
To help rule out clotting (thrombotic) episodes and to help diagnose conditions related to thrombosis
When To Get Tested?
When you have symptoms of a blood clot or a condition that causes inappropriate blood clots, such as deep vein thrombosis (DVT), pulmonary embolism (PE), or disseminated intravascular coagulation (DIC), and to monitor treatment of DIC and excessive clotting conditions
D-dimer is one of the protein fragments produced when a blood clot gets dissolved in the body. It is normally undetectable or detectable at a very low level unless the body is forming and breaking down blood clots. Then, its level in the blood can significantly rise. This test detects D-dimer in the blood.
One of the final fibrin degradation products produced is D-dimer, which can be measured in a blood sample when present. The level of D-dimer in the blood can significantly rise when there is significant formation and breakdown of fibrin clots in the body.
For a person who is at low or intermediate risk for blood clotting (thrombosis) and/or thrombotic embolism, the strength of the D-dimer test is that it can be used in a hospital emergency room setting to determine the likelihood of a clot's presence. A negative D-dimer test (D-dimer level is below a predetermined cut-off threshold) indicates that it is highly unlikely that a thrombus is present. However, a positive D-dimer test cannot predict whether or not a clot is present. It indicates that further diagnostic procedures are required (e.g., ultrasound, CT angiography).
Liver disease labs
- Protime (prolonged w/ cirrhosis)
- Liver enzymes
-AST/ALT elevated in liver damage
-ALP up if bile ducts are blocked
-albumin decreased w/ cirrhosis
normal phenomenon occurs toward end of inspiration in some people, recall that closure of aortic and pulmonic valves nearly synchronous.
Due to effects of respiration on the heart, inspiration separates timing of 2 valves' closure, and aortic valve closes 0.06 sec. before pulmonic valve.
Instead of one DUP, you hear a split T-DUB.
During expiration both valves close together.
Only heard in pulmonic valve area, 2nd ICS
S2 split causes
prolonged RV ejection time
paradoxically split (a2 following p2) = from aortic stenosis or LBBB
S4 heart sound
Stiff/hypertrophic ventricle (aortic stenosis, restrictive cardiomyopathy)
caused by late diastolic filling
Because the fourth heart sound is low in frequency, it is best heard with the bell of the stethoscope placed lightly against the chest wall.
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