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Pathophys Final pt 2

Pathophys Final- neuro, pulm, cardio, endocrine

QuestionAnswer
Spinal tracts- (info carried & direction)- Ascending 2 sensation, 2 Spinocerebellar (muscles contrax), 2 Spinothalamic (pain, temp, proprioception, fine touch, vibratory sense)
Peripheral Nervous System (components) spinal nerves, ganglia
Spinal Nerves- Afferent vs. efferent Afferent- sensory- to brain; Efferent- motor- away from brain
Spinal Nerves 31 pairs
Spinal Nerves- spinal reflex arc Respond to stimuli – protective circuitry for quick motor output; Stimulus- sensory information carried through dorsal root (afferent) to spinal cord, where motor response sent immediately through ventral root (efferent root) to skeletal muscle- response
Spinal Nerves- dermatome Specific areas of cutaneous innervation
Cerebral Lobes Frontal, Parietal, Temporal, Occipital
Frontal Concentration, abstract thought Info storage/memory Motor function Affect, judgment, inhibitions, personality Broca’s area – speech (motor control) Limbic system
Temporal Auditory Reception Interpretive area- integrate info Thinking
Parietal Sensory analysis (conveys to thalamus) Location and spatial awareness
Occipital Visual interpretation
Cerebellum (functions) coordination, balance, timing; smoothes out & coordinates voluntary muscle activity; helps in maintenance of balance and muscle tone
basal ganglia fine tuning; masses of nuclei (groups of nerve cell bodies) deep in cerebral hemispheres that are responsible for fine motor movements, especially hands and lower extremities (extrapyramidal system)
brain stem (LOC) Change in level of alertness/consciousness if injured
hypothalamus part of dienchepalon; Optic chiasm; Mammillary bodies (smell information and emotion); Link to Endocrine system, metabolism; Fluid Balance; Temperature/ BP regulation; Sleep-wake cycle; Autonomic Nervous System regulation
blood flow to CNS decreased collateral flow available
Circle of Willis collateral flow and communication; frequent site of aneurysms
arterial vs venous flow the veins reach the brain’s surface, join larger veins, then cross the subarachnoid space and empty into the dural sinuses within the dura mater. sinuses > jug vein > heart & lungs; depend on bp for flow/direction
Carotids/Vertebrals Internal Carotid Arteries >>> Cerebral Arteries Vertebral Arteries >>> Cerebral Arteries Circle of Willis (collateral flow and communication
Venous Sinuses Superficial Cerebral Veins >>> venous plexuses/sinuses >>> Internal Jugular Veins Deep Cerebral Veins >>> venous sinuses/plexuses >>> Internal jugular Veins
Blood Brain barrier (concept) Selectively guards movement of substances from blood to interstitial spaces of brain or CSF Very Important when discussing medications/drugs, etc Like a filter/sieve
Meninges (3 and spaces) Surround brain and extend to lower sacrum- Epidural Space Duramater Meninge(firm)- Subdural Space Arachnoid Meninge- Subarachnoid Space Pia Mater Meninge
CSF- function? location? what if increased? the intracranial and spinal structures “float” in to cushion and protect them; made in the choroid plexuses after components absorbed from blood supply at arachnoid layer…. Circulates (125-150 mL at a time through 4 fluid chambers) ; ICP!! BAD!
Autonomic Nervous System-(2 branches) neuromodulators/neurotransmitters and receptors; effects of stimulation Sympathetic-fight or flight; Parasympathetic- rest & digest regulated by spinal cord, brain stem, and hypothalamus; involuntary- coordinates, maintains& restores homeostasis among visceral organs, regulates cardiac/ smooth muscle tone/glands of the body.
Upper Motor Neuron Motor neurons in the cerebral cortex that control the motor neurons in the spinal cord supplying the skeletal muscles Contained completely in CNS, Fine motor, spinal reflex arcs
Lower Motor Neuron Motor neurons in the spinal cord that supply the skeletal muscles Direct muscle influence, Affect PNS and CNS, Gray matter contains
brain injury depending on what area was injured, certain symptoms will appear- for ex. coordination, vision, balance, breathing, bp, etc.
Cranial Nerves- mnemonic “ On Old Olympus Towering Tops A Fin And German Viewed Some Hops”
Cranial Nerve Function- mnemonic “Some Say Marry Money But My Brother Says Bad Business (to) Marry Money” = another mnemonic= assists to remember function of each nerve pair (s= sensory; b=both; m= motor)
Major Endocrine Organs the pituitary, thyroid, parathyroid glands, adrenal cortex and adrenal medulla, the pancreatic islets, and the ovaries and testes.
Connection with CNS release of hormones is regulated by this system
ANS synthesizes hormones
Hormones Chemical messengers
Releasing organ, target organ, and effects (Hormones) released by an organ and transported via body fluids to receptors on target organs/tissues where they exert their effect on that organ and, ultimately, on body processes.
Feedback loop principle Hormone secretion varies during a typical 24 hour period- some are released cyclically (like estrogen and female sex hormones), some are released diurnally based on the sleep-wake cycle (such as growth hormone),
Hypothalamic-Pituitary Axis closeness of the 2 allows increased control of the pituitary (and consequently other endocrine organs) by the higher cortical (CNS) centers of the body
Principle that endocrine disease may be caused by hypothalamic trauma, injury, or lesion/mass dysfunction of the hypothalmus results in altered release of hypothalmic hormones so pituitary function is also altered and endocrine functions normally driven initially by the hypothalamus do not occur.
What are manifestations of hypopituitarism? decreased ant pituitary hormones
What are the manifestations of hyperpituitarism? increased ant pituitary hormones Acromegaly Cushing Syndrome
Posterior Pituitary (organ & hormone) ADH SIADH
SIADH Syndrome of Inappropriate Antidiuretic Hormone
Manifestations of SIADH Elevated ADH; Fluid Volume Excess; Dilutional Hyponatremia; Concentrated Urine; Renin/Aldosterone attempt balance; Fluid restriction helps
What is Diabetes Insipidus? caused by insufficient posterior pituitary production of ADH so increased diuresis, Polyuria, polydipsia (but no glucose or ketones in urine as in DM b/c cause is lack of ADH, not increased blood glucose levels).
manifestations of Diabetes Insipidus Insufficient ADH; Polyuria and polydipsia; DDAVP = synthetic vasopressin (ADH)
Diabetes Mellitus? Type I and Type II. The acute complications can cause metabolic disease. risk of stroke, coronary artery disease, blindness, end-stage renal disease, and peripheral vascular disease.
TH (T3/T4) Control rate of metabolic processes, follicular cells Need iodine for production
Role of TRH from the hypothalamus, stimulates the pituitary gland to secrete TSH
Role of TSH stimulates the thyroid to produce thyroid hormones
manifestations of hypothyroidism? decreased metabolism/slowing- weak, resp distress, brady, low temp, sleep apnea, fatigue, weight gain
manifestations of hyperthyroidism? increased metabolism/ reviving; weight loss (increased appetite), HF, tachy, fatigue, tremor, anxiety
PTH Serum Ca regulation
Role of Vitamin D3 with Ca (parathyroid) it is the most active form of Vitamin D and it increases Ca and phosphate absorption in the gut and increases bone mineralization (pulls Ca into bone), and it decreases PTH so less Ca is in the serum and less Ca is lost from the bone.
manifestations of hypoparathyroidism? Tingling/ burning (paresthesias) in your fingertips, toes and lips; Muscle aches- legs, feet, abdomen or face; Muscle Spasms; Fatigue; Painful menstruation; Patchy hair loss; Dry skin; Brittle nails; Anxiety; HA; Depression; Memory problems
manifestations of hyperparathyroidism? fatigue, depression, bone pain, HTN, GERD, kidney stones
Insulin, beta cells (pancreas, hormones, effects) Secretion: chemical (blood glucose level), hormone (amino acids and GI hormones), neuro (ANS stimulation), prostaglandins; promote glucose uptake and metabolism; Liver, muscle, adipose tissue; Effected by K+ concentration
Glucagon, alpha cells (pancreas, hormones, effects) Increased blood glucose via increased glucogenolysis and gluconeogenesis; Antagonistic to insulin; Secretion: chemical (blood glucose level), neuro (ANS)
DM I vs DM II? Why do we initially treat I with insulin and II with pills instead usually? 1- beta cells are destroyed, no insulin available, so it needs to be replaced through injections; 2- beta cells are not destroyed, insulin is still available, but cells are not responding to stabilize insulin levels
signs and symptoms of DM? Polyuria (osmotic diuresis); Polydipsia; Polyphagia; Fatigue, weakness; HA; Blurred vision; Nausea; Weight changes; End-organ damage signs/sxs
hyperglycemia and why does it occur? elevated blood glucose levels
ketoacidosis high concentration of ketone bodies, formed by breakdown of fatty acids and destruction of amino acids
Adrenal Medulla the inner portion of the adrenal gland that secretes catecholamines, epinephrine and norepinephrine. Controlled by SNS; the function is NOT essential for life.
Catecholamines hormone produced by adrenal gland Epinephrine/Norepinephrine
manifestations of pheochromocytoma increased catecholamines secondary tumor of adrenal medulla. tachycardia, insomnia, flushing, increased blood pressure
Adrenal cortex (hormones & effects) Glucocorticoids Cortisol (stress hormone) Stimulated by ACTH
Mineralocorticoids (Adrenal Cortex) Aldosterone Stimulated by ACTH, Renin-angiotensin system, and Sympathetic nervous system- Na/H2O depletion; K+ excess; Decreased blood volume
Role in Na/ion transport (Mineralocorticoids) Pulls Na into epithelial cells, by turning up Na pump activity
Adrenal Sex Hormones Androgens, Estrogens; in Adrenal Cortex; triggered by ACTH
manifestations of hypofunctioning of adrenal cortex Ex- Addisons Disease weakness, fatigue, decreased blood pressure, decreased ability to respond to stress and fight infection, and GI symptoms; severe deficiency may result in death
manifestations of hyperfunctioning of adrenal cortex Cushing Syndrome emotional disturbance, hirsutism, moon facies, osteoporosis, cardiac hypertrophy and HTN, buffalo hump, obesity, adrenal hyperplasia, thin/ wrinkled skin, abdominal striae, amenorrhea, purpura, hyperglycemia, insomnia, poor wound healing
3 Layers of heart endocardium, myocardium, epicardium
4 Chambers Right Atrium, Right Ventricle, Left Atrium, Left Ventricle; Ventricles are bigger then Atria; Left Ventricle is bigger than Right Ventricle
Atrioventricular Valves Tricuspid, Mitral Close when ventricles contract (S1) Tricuspid (RA/RV) Mitral (LA/LV)
Semilunar Pulmonic, Aortic Close after ventricular contraction (S2) Pulmonic (RV/PA) Aortic (LV/aorta)
Great Vessels Superior and Inferior Vena Cava Coronary Sinus Aorta Pulmonary Artery and Pulmonary Veins
Left Main Coronary Artery Left Anterior Descending Artery (anterior wall of heart) Circumflex Artery (left lateral wall of heart)
Right Coronary Artery Right side, bottom of heart Posterior Descending Artery (posterior wall of heart)
Progress of blood flow in normal heart (deoxy) Right atrium, tricuspid valve, right ventricle, pulmonic valve, pulmonary artery, lungs, (oxy) pulmonary vein, left atrium, mitral valve, left ventricle, aortic valve, aorta, the rest of the body
Systole “squeeze” Contraction of the muscle Ventricular contraction Propels blood forward into circulation Chambers become smaller as blood ejected
Diastole “dilate” or “die” Relaxation Ventricular filling Rapid filling early and late Chambers fill with blood for subsequent ejection
dysrhythmia Caused by CHANGE; abnormalities in the conduction of the electrical current can cause dysrhythmias that produce abnormal heart rates and rhythms
Cardiac Output Stroke Volume x HR
What controls stroke volume? amt of blood ejected per heartbeat; difference between the end-diastolic volume (after filling and atrial contraction) and the end-systolic volume (after ventricular contraction
Preload amount into ventricles during filling (diastole); how much blood can you get into the heart- too much is bad- wont be able to go back to before preload size
Frank-Starling Law increased muscle fiber stretch → stronger contraction and increased stroke volume UNTIL physiologic limit of muscle met ; like rubberband
Afterload amount of resistance against which ventricles are pushing (pressure after the ventricles) – how much pressure are you using to get out of the heart
Contractility amount of squeeze of the myocardium
How does O2 deprivation affect contractility? decreased oxygen levels will initially increase contractility as compensation (to pump more blood and potentially more O2 to tissues), but severe hypoxemia (pO2 less than 50%) will decrease contractility because myocytes not getting enough O2
How do they each affect stroke volume? Cardiac output? an increase in HR will increase CO and an increase in stroke volume will increase CO
What controls and affects heart rate? Sympathetic = increases HR; Parasympathetic = decreases HR; *increase bp, decrease hr(decrease symp) ; decrease bp, increase hr;(increase parasymp)
Vasodilation and Vasoconstriction; Regulated by what? ANS, Hormones, Renin-angiotensin System, direct chemicals; vasoconstricts to decrease flow through and/or increase pressure and vasodilates to allow increased flow through and/or decrease pressure
Atherosclerosis disease/ plaque/ hardening of arteries
CAD (Coronary Artery Disease) disease and plaque build-up within arteries; decreased nourishment and oxygenation of the heart; result is decrease in blood flow and oxygen; leads to ischemia and can result in infarction of the tissue, if bloodflow is not resolved → MI
Aneurysm an excessive localized enlargement of an artery caused by a weakening of the artery wall
Capillaries Narrow, thin walled; Rapid exchange nutrients and waste btw blood stream and tissues; More capillaries where higher metabolic demand; Diameter changes passively; Single thin endothelial layer
Diffusion: Filtration and Reabsorption (capillaries) Continuous, based on hydrostatic/osmotic pressures
What is result of decreased capillary osmotic pressure at venous end? No reabsorption → edema
Veins Venoconstriction (ANS controls); Blood movement against gravity = role of skeletal muscles and one-way endothelial valves
Venous Abnormalities Venous thrombosis/DVT- blood clot in the vein
Lymph system (function) Fluid movement from tissue to venous system
BP control (Baroreceptors) (CV system itself)- (sense changes in stretch of vessel wall); Messages to CNS CV center → change HR and muscle tone
BP control (Chemoreceptors) (CNS messages)- (detect changes in O2, H+, and CO2); Messages to CNS CV center → widespread vasoconstriction
BP control (Renin-Angiotensin) increases BP
HTN Loss of reciprocal relationship btw cardiac output and vascular resistance; Increased fluid volume and/or peripheral resistance with no change in other to compensate for this
HTN (primary) characterized by a chronic elevation in BP that occurs without evidence of other disease (unknown)
HTN (secondary) by an elevation of BP that results from some other disorder, such as kidney disease (known)
Ischemia/Infarction Deficient blood supply to a body part (failure to dilate in response to increased need for blood flow or failure to supply needed blood and O2 to tissue)
Myocardial Ischemia (what happens?) Insufficient flow of or O2 content of blood to meet myocardial cell demands; decrease- ability to contract, pump function, glucose source, aerobic metabolism; increase- anaerobic processes & lactic acid
Myocardial Ischemia (pain? end result?) death of tissue, loss of function; resolve with reperfusion and O2 demands met OR infarction)
Ventricular Hypertrophy What is it?- enlargment of ventricles → scarring→ thickness of heart; What can cause it?- stress, disease, HTN; Why is it a problem?- impairs filling → diastolic dysfunction
Cardiomyopathy Impaired cardiac output, irreversible myocyte damage- loss of function
Cardiomyopathy (types) Dilated- Significant dilation of ventricles, poor systolic function; BIG; Hypertrophic- Asymmetric thickening of heart, poor diastolic function; Obstructive or Nonobstructive; THICK Restrictive- Rigid ventricular walls, poor diastolic function; STIFF
Heart Failure Inability of heart to pump sufficient blood to meet the needs of tissues for O2 and nutrients
HF (Left- sided, S&S?) tachycardia, dysrhythmias, tachypnea, orthopnea, anxiety, cyanosis, decreased BP and peripheral pulses, crackles, wheezes, S3/S4 gallop, apical murmurs, elevated pulmonary capillary wedge pressures, and decreased CO
HF (Right-sided, S&S?) dependent edema, JVD, bounding pulses, oliguria, dysrhythmias, HSM, increased CVP, and altered LFTs
HF (causes) The LV loses ability to eject blood into the systemic circ > large volume of blood remaining in the LV after systole. Backup of the blood may progress to the LA, then to the pulmonary system (L HF) > RV & RA, and finally to the systemic circulation (R-HF)
“cor pulmonale” pulmonary heart disease; enlargement of right ventricle
Ventilation movement of air in and out Perfusion = CV System
Diffusion movement of gas molecules by exchange from area of high concentration to area of lower concentration
Upper Respiratory Tract Warms, filters Nose, sinuses/nasal passages, pharynx (nasopharynx- adenoids; oropharynx- tonsils; laryngopharynx- epiglottis) larynx, trachea, turbinate bones
Lower Respiratory Tract Gas exchange Lungs- Lobes; Bronchi- Carina, Hila, Goblet Cells; Bronchioles; Alveolar Ducts; Alveoli- Surfactant, Alveolar Macrophages Mediastinum Pleura
Pulmonary Circulation Less pressure/resistance than systemic circulation Pulmonary Artery (1 to) Arterioles → capillary beds alongside basement membranes of alveoli → gas/nutrient/waste exchange Pulmonary Veins (2 away) Venules → veins → LA of heart (oxygenated blood)
Bronchial circulation Systemic circulation – nourishes lung tissue and pleura Drains into systemic veins/sinuses and pulm vein
Lymphatic vessels deep and superficial Removes fluid
Ventilation Movement of air in and out of airways
Ventilation- controls/mechanics Mechanics- Air-pressure variances, Resistance to air flow, Lung compliance Neurochemical Control- Respiratory center of brain (Medulla and Pons) Peripheral chemoreceptors, lung receptors, central chemoreceptors Autonomic nervous system innervation
Ventilation- factors surface tension of alveoli (normally low with surfactant); connective tissue (collagen/elastin) of lungs
Ventilation- normal compliance lungs easily stretch and distend when pressure applied = normal “elastic recoil”
Ventilation- increased compliance overdistention, decreased elasticity (ex: emphysema) ex. Hairband
Ventilation- decreased compliance stiff (ex: pulmonary fibrosis)…. Blowing glass as getting colder→More energy needed to ventilate less compliant lungs
how does compliance affect ventilation The nervous system controls the movement of the respiratory muscles and adjusts the rate of breathing so it matches the body needs during various activities and varying needs for O2 supply and CO2 removal
Hyperventilation increase rate and/or tidal volume; too much CO2
Hypoventilation decrease rate and/or tidal volume; Not enough CO2
Diffusion O2 and CO2 exchange @ air-blood interface Alveolar-capillary membrane Thin alveolar membrane + large surface area Movement per gradients- Diffusion down concentration gradient
Diffusion types of gases O2- Air → plasma (across alveolar-capillary membrane) → 98% into RBC onto hemoglobin, 2% remains in plasma; Diffusion continues until PaO2 in plasma = PAO2 alveoli CO2- More efficient and quick diffusion/transfer; Plasma → alveoli and out with expiration
Diffusion- gas principles O2-Carried free in plasma or mainly on hemoglobin; Affinity of hgb for O2 changes based on tissue demands for O2 CO2- Dissolved in plasma (10%), bound to hemoglobin (30%), or carried as bicarb in plasma (60%)
Perfusion Blood flow thru pulmonary circulation factors- Pulmonary Artery Pressure (RV force and PA properties); Gravity; Alveolar Pressure
Hypercapnia Increased CO2 in arterial blood (increased PaCO2) Induced by hypoventilation treat- non-invasive positive pressure ventilation (CPAP, BiPAP) intubation and mechanical ventilation
Hypoxemia Decreased oxygen level of arterial blood (decreased PaO2); Decreased O2 delivery to alveoli, Decreased diffusion of O2 into blood, Lack of perfusion of pulmonary capillaries
Hypoxia deficiency in the amount of oxygen reaching the tissues
Acute Resp Failure Severely inadequate gas exchange (O2 and/or CO2) Manifestations- Tissue Hypoxia, CNS effects/decline, Death Treatment- Supplemental O2 and/or ventilatory assistance
Bronchiolitis Inflammatory obstruction of small airways (bronchioles); More common in children; Potential destruction distal to inflammation if severe Increased in peds patients; often viral etiology
Bronchitis Usually viral etiology- Inflammation of bronchi, usually viral; Cough, sputum, possible mild obstruction, self-limiting usually
Pneumonia Streptococcus pneumoniae Inflammation, immune complex activation; Microorganism may release toxins directly that cause tissue damage
Pneumonia- manifestations Edema and infiltration of bronchial walls, increased fluid and debris in alveoli → sputum, cough, dyspnea, fever, decreased diffusion (VQ mismatch) → hypoxemia
Aspiration entry of secretions/ foreign material into lungs Risk- decreased LOC, instead of swallowing in to GI, food, fluids, saliva will drop into lungs→ infection, possibly “drown” if not caught prevent by- Coughing, swallowing, ET tube, thicken fluids
TB Airborne-droplet transmission manifestations- Bacterium lodge in lung tissue → nonspecific pneumonitis and lymphatic involvement; Bacilli engulfed and form granulomatous lesions, then necrosis of lung and scarring Systemic sequelae possible
Lung dx- Restrictive Decreased compliance; Increased work of breathing→Dyspnea- RR and Tidal Volume; Alveolocapillary Membrane changes→ Decreased diffusion→ Hypoxemia
Lung dx- Obstructive Airway obstruction (expiration); Increased force of expiration; Emptying of lungs slowed → Use of accessory muscles, Dyspnea, Wheezing (obstruction); Increased work of breathing; Ventilation/Perfusion mismatching; Decreased FEV1
Pulmonary Fibrosis Excessive amt of fibrous or connective tissue within the lung Why considered “restrictive”? Stiff and noncompliant lung, Decreased ventilation, Decreased diffusion @ alveolocapillary membrane, Hypoxemia
ARDS Acute respiratory failure; Injury to pulmonary cap endo; Diffuse inflammation→ cascade initiated Diffuse alveolocapillary membrane damage; ↑ cap permeability → pulm edema Injury to alveolar epithelium- ↑ alveolar fluid, ↓compliance, ↑ risk of infectio
ARDS (Why restrictive) Pulmonary edema, hypoxemia, shunting of blood flow, increased work of breathing
Asthma Type I hypersensitivity response- rxn to allergens/irritants Bronchial inflammation and smooth muscle spasm; Eosinophils contribute to inflammation and tissue damage; Vasoactive mediators→ vasodilation and capillary permeability
Asthma (Results/ Risks) Bronchial spasm, vascular congestion, pulmonary edema, thickened airway walls, increased hyperresponsiveness of bronchi; Acute respiratory failure; Long-term irreversible airway damage
COPD Expiratory obstruction caused by progressive airflow limitation that is not fully reversible Abnormal inflammatory response of lung to noxious particle/gas; Mucus plug formation and bronchial wall collapse → airtrapping
COPD- cont'd inflam of epithelial lining of airway→ Infiltration of inflam mediators in bronchial walls; Inhibit antiproteases→ loss of elastic recoil; Edema and mucus ↑ → infection risk Obstruction, alveolocap changes, ↓ diffusion, ↑ infection/bronchospasm
Emphysema Inhibition of antiproteases (further inflammation and breakdown of elastin) → loss of elastic recoil of bronchial walls Continuous bronchial irritation and inflam→ chronic bronchitis → edema, ↑ mucus secretion, infection risk
Airtrapping abnormal retention of air in the lungs after expiration. Manifestations- emphysema, COPD, bronchitis, etc
COPD- general manifestations mucus, loss of recoil, and ↓ diffusion → dyspnea, cough, hypoxemia, hypercapnia, and ultimately cor pulmonale b/c ↑ pressure in pulmonary arterial system.
Pneumothorax Air or gas in pleural space → partial or total lung collapse
primary vs second pneumo occurs in the absence of known lung disease, occurs in someone with underlying lung disease (COPD)
Open vs tension pneumo injury ex. GSW opening that allows air to enter the pleural space functions like a valve, and with every breath more air enters and cannot escape
Plueral Effusion accumulation of fluid between the layers of tissue that line the lungs and chest cavity Classification based on type of cells present in fluid
Lung CA Bronchiogenic- Arises from epithelium of respiratory tract Same as pathophysiology of tumor spread- Consumes space in lung, Local destruction, then extending destruction Small Cell Carcinoma Non Small Cell CA-Squamous, Adenocarcinoma, Large-Cell Carcin
Pulmonary HTN Increased pulmonary artery pressure May be r/t pulmonary or cardiac disease origin “Cor Pulmonale”
Pulmonary Embolism Obstruction of blood flow through pulmonary circulation; Most common origin = DVT; Clot (thrombotic), air, fat, or amniotic fluid
What injured areas might cause impaired motor activity? Impaired motor coordination? Frontal; Cerebellum
ACTH secreted by pituitary gland; stimulates the adrenal cortex
GH secreted by pituitary gland
Prolactin anterior pituitary gland, stimulates milk production after childbirth
FSH secreted by anterior pituitary; promotes production of ova/sperm
TSH synthesized/ produced in anterior pituitary; regulate endocrine function of thyroid
LH secreted by anterior pituitary; stimulates ovulation in females and the synthesis of androgen in males
Created by: sccrgrl159 on 2010-10-18



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