study guide

• diabetes type 1 is damage to beta cells so not enough insulin, autoimmune disorder

  • there will be diabetic ketoacidosis which is acetone formed
  • causes kussmal respirations
  • polyuria
  • polyphagia
  • polydipsia
• diabetes type 2 is decreased beta cell response to glucose levels and insulin resistance

  • no or less severe acidosis
• Hypertension

  • Increased activity of RAAS
  • Angiotensin I converted to angiotensin II in lungs (angiotensin converting enzyme: ACE)
  • Angiotensin II is a potent vasoconstrictor: increased PVR  -vasoconstrictor narrows lumen and increases resistance and pressure
  • Circulating angiotensin II stimulates aldosterone secretion
  • Aldosterone causes retention of Na+ and water → Increases blood volume
• Atherosclerosis

  • Oxidation of LDL cholesterol in blood  - Occurs because of adhesion to the macrophages
  • Factors that promote atherosclerosis: smoking, diabetes, hypertension, low levels of
  • HDL, high levels of LDL, increased serum triglycerides
  • Oxidized LDL allows entry of monocytes & T lymphocytes
  • Large amounts of consumed LDL transformed into foam cells- Foam cells accumulate
• atherosclerosis

  • Multiple foam cells form a fatty streak - Fatty streak is primary component of atherosclerosis (the lesion)
  • Formation of fibrous cap around cholesterol core
  • Necrotic core = unstable plaque = vasospasm & platelet aggregation
  • Necrotic areas accumulate calcium deposits  -hardening occurs, unstable plaque can rupture
  • Rupture, hemorrhage of plaque à triggers clotting cascade - can drop blood flow and increase the pressure because of a clot in the lumen
• Myocardial infarction

  • Electrocardiographic changes -electrical conduction changes in necrotic area
  • ST segment depression or T wave inversion
  • Non-ST-segment elevation MI (NSTEMI) or subendocardial injury -where ST segment is depressed  -ST segment depression or T wave inversion is ischemia (lack of blood flow)
  • ST segment elevation: ST-segment MI (STEMI)
  • Transmural injury -ST segment elevation is classic heart attack 
• Angina

  • Ischemic heart produces lactic acid → stimulation of nerve endings
  • Typical pain: pressure -sometimes burning, heavy, squeezing, pressure, radiating pain
  • radiation
  • Associated symptoms: nausea, diaphoresis, weakness, pallor, lightheadedness and shortness of breath (dyspnea)
• Myocardial infarction

  • troponin
• Atrial Fibrillation: disorganized, rapid depolarization of atrial tissue (very common)

  a.           Rates often > 300 bpm

  b.           Impulses are randomly conducted to ventricles -irregular pulse

  c.           Heart failure often associated with a. fib

  d.           Risk for thrombosis

  e.           Common causes: heart disease, alcohol intoxication, caffeine, electrolyte imbalances
• Ventricular Fibrillation

  a.           Disorganized, chaotic electrical activity originating in the ventricles

  b.           Associated with myocardial ischemia

  c.           No effective cardiac output

  d.           Life-threatening, patient unconscious, pulseless

  e.           Poor survival rate unless defibrillation occurs immediately -medical emergency!!!!
• First Degree Heart Block

  a.           Atrial impulse slowed through the AV junction -longer PR interval

  b.           Conducted through to the ventricles consistently
• Second Degree Heart Block: Type I (Wenckebach)

  a, Progressively greater delay in conduction through the AV junction -progressively longer and longer and..

  b.           Eventually an impulse is blocked

  c.           Repeating cycles
• Second Degree Heart Block: Type II

  a.           Intermittent non-conduction through AV junction

  b.           Slower ventricular rate

  c.           Decreased pulse and CO
•  

  Third Degree (Complete) Heart Block

  a.           All atrial impulses are blocked

  b.           No association between atrial and ventricular conduction

  c.           Decreased heart rate and CO -tired, fatigue, loss of consciousness
• causes of heart blocks

  a.           Damage to AV junctional tissue → MI, heart disease

  b.           Drug effects or electrolyte issues
• Stenosis: narrowing, stiffens

  • Valve stiffens – opening affected (more force required to push blood through)
  • Resistance and obstruction of flow
  • Increased workload of chamber pumping blood through narrow opening 
  • Murmur
  • Chamber enlargement: hypertrophy
  • Decreased cardiac output and heart failure (leads to valve replacement surgery)
• Regurgitation: insufficiency; backflow

  • Valve leaflets close incompletely
  • Blood is shunted backward→ Murmur
  • Increased pressure and enlargement of chamber
  • Increased workload
  • Decreased CO → heart failure
• Pathophysiology of Acute Pericarditis

  • Inflammation → Fluid accumulation (specifically in pericardial space
  • Formation of exudate part of inflammation, creates pressure on heart
  • Decrease in venous return because of pressure
  • Decrease in cardiac output (due to pressure)
• Pathophysiology of Chronic Pericarditis (often secondary to trauma or neoplastic disease)

  • Fibrosis (scar tissue) of pericardial sac
  • Tightening of scar tissue around heart
  • May form adhesions connections from scar tissue where there shouldn’t be connections 
  • Decreased efficiency as a pump → signs of failure
• Pericarditis: acute or chronic inflammatory process of visceral and/or parietal pericardium -around the heart; pericardium lubricates and protects the heart

  • May spread to or from myocardium (myocarditis) will affect the pumping of the heart
  • Etiology
  • Microorganisms (typically bacterial (sometimes viral)
  • Complication of disease (MI, autoimmune disease, cancer)
  • Heart trauma (open heart surgery is one of the leading causes of pericarditis
• Clinical Manifestations of pericarditis

  • Pericardial friction rub  sound of pericarditis, can hear with stethoscope, distinct rubbing sound
  • Chest discomfort (very severe pain, sharp with breathing)
  • Fever
  • Pericardial effusion: fluid between pericardium & myocardium
  • Cardiac tamponade -fluid in pericardial space, causes pressure on heart, and decrease CO (muffled heart tones)
• Pathophysiology of respiratory failure

  Respiratory Failure: clinical syndrome with many different causes

  • Defined: inability of the pulmonary system to oxygenate blood or remove CO2
  • Hypoxemia: decrease in oxygen in the blood
  • Hypercapnia: increase of carbon dioxide in the blood typically from inadequate breathing
• Manifestations of respiratory failure

  • Arterial blood gases indicating hypoxemia &/or hypercapnia
  • Respiratory acidosis initially: increase in carbon dioxide
  • Increased anaerobic metabolism → Metabolic acidosis
  • Increased work of breathing, shortness of breath (dyspnea)
  • Increased heart rate
  • Cyanosis
  • Clubbing of nails
  • Erythropoietin release
  • bone marrow increase RBC production
  • Hypoxia -> renal failure
  • All body systems involved: tissues become hypoxic
  • Carbon dioxide narcosis
  • Dilation of cerebral blood vessels
  • Increased blood flow to the brain = IICP
  • Confusion-coma-death
• Asthma

  • Pathophysiology
  • Stimulus (often allergen) or exercise induced
  • Cellular mediators: histamine, leukotrienes, interleukins, prostaglandins =               bronchoconstriction
  • Acute phase: primarily bronchoconstrictive: tight airways
  • Airway obstruction due to inflammatory swelling
  • Late phase: mucous and edema cough develops
  • Increased airway resistance from narrowing
• Asthma

  • Clinical Manifestations depend on degree of obstruction
  • Tachypnea and cough
  • Wheezing decreased air movement
  • Chest tightness worse with deep breath
  • Hypoxemia and hypercapnia late if the asthma doesn’t respond to meds
  • Status asthmaticus severe sustained episode; can be life-threatening
• Emphysema

  • Pathophysiology: repeated exposure to irritant causes repeated inflammatory response with scarring things like smoking and poor air quality
  • Proteases produced: digest elastin in the alveolar walls
  • Loss of antiprotease α1 antitrypsin due to the stimulus
  • Elastin network breaks down = Loss of elastic recoil lungs ability to deflate after inhalation
  • Alveolar damage: enlargement and destruction = air trapping -> Hyperinflation of lungs
  • Airway inflammation = mucous production
  • Support structures of airways lost
• Emphysema

  • Clinical Manifestations
  • Dyspnea and cough often productive cough
  • Increased chest diameter enlargement of alveoli
  • Use of accessory muscles, chronic hypercapnia CO2 are greater than 50
• Pulmonary embolism

  • Pathophysiology
  • Clot lodges in pulmonary vessel → abrupt increase in pulmonary vascular resistance due to occlusion; sudden occlusion that causes the release of mediators
  • Mediators causing vasoconstriction: Pulmonary artery hypertension
  • Rise in right ventricular pressure
  • Increased amount of pulmonary dead space = Ventilation/perfusion mismatch; perfusion is not occurring
  • Loss of surfactant due to decreased blood flow to surfactant producing cells- cause atelectasis which is alveoli collapse
  • Bronchoconstriction from release of serotonin from platelets
• pulmonary embolism

  • Clinical Manifestations
  • Range from no symptoms to cardiovascular collapse
  • Dyspnea, chest pain, often sudden onset; hurts most with deep breath
  • D-dimer: measurement of fibrin degradation fragment; will be elevated if there is a clot somewhere
  • CT scan; shows abnormality in blood flow, very useful
• Head trauma

  • Pathophysiology
  • Primary injury: varies trauma itself (can be minimal or very severe)
  • Minimal disruption confusion, concussion
  • Extensive disruption severe neurological defects
  • Secondary injury more serious than impact itself
  • Inflammation: closed space caused increased intracranial pressure
  • Cerebral edema vessel compression (lack nutrients and oxygen)
  • Intracranial bleed/hematoma hemorrhaging, clots; subdural, epidural, intracerebral; IICP)
• Meningitis pathophysiology

  • Organism replicates in the CSF releases toxins
  • Organism stimulates inflammatory response → Increased intracranial pressure due to inflammation and exudate
• Types of seizures

  C. Focal Seizures partial seizures that come from one area : simple partial seizures means individual maintains awareness

  • Focal motor: begin locally in premotor cortex
  • Contraversive movement eyes/head turn away from area that is affected 
  • Begin distally can progress up the body
• Types of seizures

  C. Focal Seizures

  • Focal sensory
  • Lesion in sensory cortex of parietal lobe
  • Simple, auditory, tactile or visual experience
  • Numbness, tingling sensation “water or spider running down arm”
• types of seizures

  Focal seizures

  • Psychomotor complex partial seizure; some anemisa or unawareness
  • Involves temporal lobe, medial surface of the hemispheres, limbic system
  • Exhibit bizarre behavior, exaggerated emotionality
  • Attitude, attention span, behavior or memory dream-like state
  • Automatisms grunting, chewing, lip smacking (action without intention)
• types of seizures

  Generalized Seizures: both hemispheres involved temporary, loss of consciousness, amnesia,

  • Absence (Petit mal): nonconvulsive
  • Symptoms: loss of awareness, staring while maintaining posture
  • May occur several times per day few second pause then resume
  • Automatisms may occur
• types of seizures

  generalized seizures

  • Tonic-Clonic (Grand mal) classic seizure, generalized so both sides of brain involved
  • Etiology: rapid, high amplitude discharge
  • Aura warning sign, bright light, smell, auditory,
  • symptoms: loss of consciousness, generalized contractions of all muscles
  • Tonic phase: rigidity jaw clenches, eyes roll back, patient doesn’t breath
  • Clonic: movements become jerky muscles contract and relax, incontintiance
• • Post-ictal state after seizure; altered state of consciousness, drowsy or confused, cant remember what happened
• • Status epilepticus life threatening stage of continuous seizure (common with alcohol withdrawal or poor medication compliance)
• Secondary or symptomatic seizures something else going on in the body causes seizure

  • Metabolic disorder acidosis, electrolyte imbalance, renal failure
  • Structural disorder tumor, brain bleed, hemorrhage, not pathophys of tradional seizures
• Schizophrenia: psychosis with disruption of thought processes; brain tissue loss/changes

  • Inherited gene defects; prenatal injury (when its not genetic)
  • Dopamine hypothesis: imbalance between dopamine and serotonin medications that block dopamine receptors are effective