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Test 4 Stuff (bruzz) Flashcards

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1
Q

What’s endocarditis?

A

Inflammation of endocardium
Caused by bacteria, viruses, fungi, ricketsia, parasites

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2
Q

Classic Findings of endocarditis

A

Fever
New or changed cardiac murmur
Petechial lesions of the skin , conjunctiva, and oral mucosa

Characteristic physical findings:
Olser nodes
Janeway lesions

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3
Q

What is rheumatic fever?

A

Systemic inflammatory disease
Streptococcal infection causing autoimmune response against molecularly similar self antigens in the heart, muscle, brain, and joints, causing an autoimmune response leading to inflamatory lesions in these tissues

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4
Q

Major clinical manifestations of rheumatic fever

A

Carditis: Murmur , chest pain, pericardial friction rub, ECG changes, valvular dysfx

Polyarthritis: Heat, redness, swelling, and joint pain

Chorea: Sudden, aimless, irregular, involuntary movements

Erythema Marginatum: Nonpruritic, erythemateous macules on the trunk that may fade on center

Subcutaneous nodules: Palpable nodules over bony prominences and extensor tendons

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5
Q

What is Frank Starling Mechanism? (heart failure)

A

Heart stroke volume increases in response to increased blood volume in ventricles

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6
Q

What is systolic heart failure?

A

EF is less than 40%
Inability of heart to generate adequate cardiac output to perfuse tissues
Stroke volume:

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7
Q

Manifestations of Left heart failure

A

Cough of frothy sputum
pulmonary edema
S3 gallop

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8
Q

What is diastolic Heart Failure?

A

Impaired filling of the heart during diastole

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9
Q

What are the types of Valvular Dysfunctions?

A

Valvular Stenosis
* Aortic Stenosis
* Mitral Stenosis

Valvular Regurgitation
* Aortic Regurgitation
* Mitral regurgitation
* Tricuspid regurgitation

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10
Q

Causes of aortic stenosis ?

A

Congenital bicuspid valve
Degeneration with aging
Inflammatory damage caused by rheumatic heart disease

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11
Q

What happens in aortic stenosis?

A

The orifice of the valve narrows causing resistance to blood flow from the left ventricle to aorta

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12
Q

True or False: Left ventricular hypertrophy occurs to compensate for increased workload in Aortic Stenosis?

A

TRUE

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13
Q

Treatment of Aortic Stenosis

A

Vasdilator therapy to reduce ventricular ejection
Surgical valve replacement

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14
Q

What does Mitral Stenosis do ?

A

Impairs the flow of blood from the left atrium to left ventrical

Results in incomplete empyting of the left atrium and elevated atrial pressure , continued increases in left atrial volume, atrial dilation and hypertrophy

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15
Q

What can mitral stenosis lead to?

A

A Fib
Thrombus formation
Pulmonary Hypertension
Pulmonary Edema
Right Ventricular failure

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16
Q

What does aortic regurgitation result from?

A

Inability of aortic valve leaflets to close properly during diastole
Some blood flows back into left ventricle
Leads to ventricular dilation and hypertrophy and heart failure can develop

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17
Q

Priimary and Secondary causes of aortic regurgitation

A

Primary: Congenital bicuspid valve or degeneration in elderly lol

Secondary: Chronic Hypertension, rheumatic heart disease, Bacterial endocarditis, syphillis, Connective tissue disease, appetitie suppressing medications, trauma, atherosclerosis

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18
Q

Manifestations of aortic regurgitation

A

Widened pulse pressure resulting from increased stroke volume and diastolic backflow ; can play a role in eye and kidney damage

Murmur in the 2nd, 3rd, or 4th intercostal spaces parasternally
Dysrhythmias

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19
Q

What does Mitral Regurgitation do?

A

Permits backflow of blood from left ventricle into left atrium during ventricular systole

Left atrium and ventricle become dilated and hypertrophied leading to heart failure

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20
Q

Symptoms of mitral regurgitation

A

Murmur ; heard best at apex and that radiates into back and axilla

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21
Q

What mostly causes tricuspid regurgitation?

A

Pulmonary Hypertension and dilation of right ventricle which pulls the valve leaflets apart

Can lead to volume overload in the right atrium and left ventricle, increased systemic venous blood pressure, and right heart failure

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22
Q

How does preload and afterload effect renal or hypertension?

A

Preload: Increases with decreased contractility or an excess of plasma volume; decreased ejection fration ; leads to renal failure, mitral valve disease

Afterload: Leads to hypertension ; decreased renal perfusion and increase in renin and angiotensin

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23
Q

What can cause right side heart failure?

A

Pulmonary diseases ; COPD, cystic fibrosis, ARDS

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24
Q

What kinds of shock are there and what’s their cause?

A

Cardiogenic: Heart failure or MI
Hypovolemic: Insufficient intravascular fluid volume
Neurogenic: Neural alterations of vascular smooth muscle tone
Anaphylactic : Immunologic process
Spetic: Infection

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25
What is cardiogenic shock?
Decreased cardiac output and tissue hypoxia in presence of adequate intravascular volume
26
What are the compensatory systems of cardiogenic shock?
Renin angiotensin aldosterone and ADH to maintain blood volume or increase Adrenal gland releases catecholamines like epi and norepi which causes vasoconstriction and increase contractility of heart
27
Hypovolemic shock happens when intravascular volume decreases by how much?
15%
28
What are the compensatory mechanisms of hypovolemic shock?
1. HR and SVR increase, boosting cardiac output and tissue perfusion presures 2. Interstitial fluid moves into vascular compartment 3. Liver and Spleen add to blood volume by releasing stored red blood cells and plasma 4. Renin stimulates aldosterone release 5. ADH increases water retention
29
What is neurgenic shock?
Widespread vasodilation Results in relative hypovolemia ; blood volume has not changed but SVR decreases so amount of space containing blood has increased
30
What can cause neurogenic shock?
Trauma to spinal cord or medulla Depressive drugs, anesthetic agents, severe emotional distress and pain
31
Symptoms of neurogenic shock?
Hypotension Bradyarrhythmia Lushed Mental status changes
32
Anaphylactic Shock symptoms
Vasodiltion and relative hypovolemia Anxiety Dizziness Diff breathing Stridor Hives Swollen Lips and Tongue
33
How to treat anaphylaxis
Epi FLuids Antihistamines and corticosteroids Vasopressors and bronchodilators
34
Septic Shock symptoms
Systemic inflammation leading to systemic inflamatory response syndrome ; fever, tachycardia, tachypnea, elevated WBC Early Stage: Hyperdynamic phase characterized by widespread vasodilation with compensatory tachycardia and increased cardiac output Later stage: Decreased Myocardial contractility, cardiac output, and tissue perfusion
35
What are signs of organ failure due to sepsis?
Increased serum lactate Thrombocytopenia Hypotension Hyperglycemia Coagulalation abnormalaties Increased bilirubin Oliguria Ileus
36
How is thermoregulation maintained?
Heat production Heat Conservation Heat Loss
37
What part of brian regulates body temp?
Hypothalamus
38
Peripheral thermoreceptor examples
Skin Liver SKeletal muscle
39
Central thermoreceptor examples
Hypothalamus SPinal cord VIscera
40
How does hypothalamus regulate body temp?
Stimulates anterior pituitary to releasse thyroid stimulating hormone
41
Hypertonia sub group things
Spasticity: gradual increase in tone Gegenhalten: Resistance to passive movements Dystonia: SUstained involuntary muscle contraction Rigidity: Muscle resistance to passive movement of rigid limb that is uniform in both flexion and extension
42
What is Hyperkinesia?
Excessive purposeless movement
43
What is Paroxysmal Dyskinesias?
Rare involuntary movements that occur as spasms
44
Types of Paroxysmal Dyskinesias
Dystonia: Uncontrollable twisting, repetitive movement resulting in abnormal posture Chorea: Abnormal jerky movements Athetosis: Slow, irregular, twisting movements most obvious in distal extremitites Ballism: Combination of all deez
45
What's Tardive Dyskinesia?
Involuntary movement of the face, lip, tongue, trunk, and extremities Can result as a side effect of antipsychotic therapy
46
What's the most common symptom of tardive dyskinesia?
Rapid, repetitive, stereotypical movements Continual chewing with intermittent protrusions of the tongue, lip, and facial grimacing
47
What is tourette syndrome?
Hallmark is presence of motor tics and vocal tics Sensory tics: Unplasant sensations in face, head, and neck areas
48
What is Huntington Disease?
Autosomal Dominant hyperkinetic disorder of chromosome 4 Severe degeneration of basal ganglia specifically the caudate nucleus There is a depletion of GABA
49
Symptoms of Huntingtons Disease
Progress over 15-20 years Involuntary hyperkinetic movements like chorea, athetosis, ballism Cognitive defects: SLow thinking, loss of memory, reduced capactiy to plan organize or sequence Restlessness, disinhibilitation, irritibility are common Apathy, depression , anxiety may follow
50
What is hypokinesia?
Loss of voluntary movement despite normal consciousness and peripheral nerve and muscle function
51
Types of hypokinesia?
Akinesia: Decrease in voluntary and associated movements Bradykinesia: Slowness of voluntary movements Loss of associated movement: Expressionless face, statue like posture, absence of speech, reduction in arm and shoulder movements
52
What is Parkinson Disease?
Depletion of dopamine Excess of cholinergic activity
53
SYmptoms of parkinsons
Hypokinesia Hypertonia Resting remor, rigidity, bradykinesia/ akinesia, postural disturbance, dysarthria, dysphagia Urinary urgency, sleep disorders, Nonmotor symptoms: Inappropriate diaphoresis, ortho hypo, drooling
54
What are upper motor neuron syndromes?
Result from injury to motor pathways that descend from motor cortex Can result from trauma, stroke, or tumors
55
Types of upper motor neuron syndromes
Paresis: Partial paralysis with incomplete loss of muscle power Paralysis
56
Types of upper motor neuron paralysis
Hemiparesis/ Hemiplegia: Paresis/ paralysis of upper and lower extremities on one side Diplegia: Both sides of body as a result of cerebral hemisphere injuries Paraparesis/ Paraplegia: Lower extremities as a result of lower spinal cord injury Quadriplegia: Paresis of all 4 extremities as a result from upper spinal cord injury
57
What are lower motor neuron injuries?
Result from injury to alpha motor neurons Impair voluntary and involuntary movements
58
Types of lower motor neuron injuries
Flaccid paresis: Hypotonia and is accompanied by hyporeflexia or areflexia Fasciculations: Muscle rippling or quivering under the skin because of muscle denervation ; tend to atropht over months Fibrilation: Contraction of a single muscle fiber because of metabolic changes in denervated muscle
59
What is guillain barre syndrome?
Acquired inflammatory disease that causes demyelination of peripheral nerves Usually caused by respiratory or GI infection
60
Symptoms of guillain barre syndrome
Tingling Weakness Paralysis of leg Quadriplegia Respiratory insufficiency Autonomic nervous system insufficiency
61
How long does it take usually to recover from guillain barre syndrome?
Within weeks or months Or up to 2 years
62
What is amytopic lateral sclerorsis?
Neurodegenertive disorder involving upper and lower motor neurons Disease in brain and spinal cord Typically diagnosed between 40-60 Usually spares sensory neurons
63
Symptoms of ALS
Muslce weakness in arms and legs DIfficulty with cordination Progresses to repsiraotry failure
64
What kinds of posture disorders are there?
Dystonia: Abnormal posture through muscle contractions Dystonic: When dystonia lasts for long time Decorticate: Arms flexed inwards, hands clenched, legs extended Decerabate: Rigid muscles, extended arms and legs, arched back Basal Ganglion: Stooped, hyperflexed posture with narrow based, short stepped gait
65
What are the disorders of gait?
Spastic gait: Shuffling, leg extended and held stiff Cerebellar/ Ataxic: Wide based with feet apart and turned outward or inward Basal Ganglion Gait: Broad Based Gait ; walks with small steps and decreased arm swinging, associated with parkinsons Frontal Lobe Ataxic: Slow walking, freezing, start hesitation
66
What are the disorders of expression?
Hypermimesis: Pathological Laughter or crying ; right hemisphere injury if laughte; left hemisphere if crying Hypomimesis: Aprosady ; Loss of emotional language, can be receptive or expressive Apraxia: Disorder of learned skill movement with difficulty planning and executing coordinated motor movements
67
What is spinal shock?
Manifestation of spinal cord trauma Normal activity of spinal cord ceases at and below level of injury
68
Manifestations of spinal shock
Complete loss of reflex function Flaccid paralysis Abscence of sensation Incontinence Transient drop in BP Bradycardia Poor venous circulation
69
What is multiple sclerosis?
Chronic and progressive CNS autoimmune inflammatory disease that effects peripheral nervous system Demyelinating disorder that disrupts nerve conduction
70
Symptoms of Multiple Sclerosis
Paresthesia Impaired giat Urinary Incontinance Visual Impairment Cerebellar And Corticospinal involvment: Nystagmus, ataxia, weakness, with all 4 limbs involved
71
What is myasthenia gravis?
Aquired Chronic Autoimmune Disease Muslce of the eye, face, mouth, throat, and neck are effected first IgG antibody produced against acetylcholine receptors
72
Myasthenic and Cholinergic crisis
Very similar Severe muscle weakness causing quadraplegia Resp insufficiency Extrememe Diff in swallowing Rise in BP, Tachy cardi, Tachypnea
73
What is NREM sleep?
75- 80 % of sleep time Brain stem coordinates activity between spinal cord and various reflexes Quiet type of sleep Relatively inactive but fully regulating brain Fully moveable body Sympathetic tone decreased but parasympathetic activity increased ; decrease in metabolic rate, temperature, HR, respiration, BP, muscle tone
74
What is REM sleep?
EEG similar to an awake person Loss of muscle movements Vivid dreams Motor systems inhibited BP, HR, Respirations increase and fluctuate, temp regulation is lost Cerebral blood flow and metabolic rate decrease Brain highly active
75
What is sleep apnea?
Central: Uncommon Obstructive: Caused by upper airway obstruction
76
Manifestations of sleep apnea
Noisy snoring Insomnia Abnormal Movements during sleep Morning Headaches Excessive daytime sleepiness
77
Treatment of sleep apnea
Behavioral Methods Positive pressure by a nasal or naso-oral CPAP
78
Traumatic vs nontraumatic brain injury
Traumatic: External force like getting hit Nontraumatic: Strokes, infections, lack of oxygen
79
What's excitatory amino acid injury?
Brain injury leads to an overabundance of excitatory amino acids Excessive glutamate: Cause uncontrolled influx of sodium, potassium, and especially calcium ions into neurons
80
Signs of brain injury
Alterations in cognitive, sensory and motor function Changes in LOC: FOcal injury and Infratentorial (brain stem) Cheyne strokes breathing Decorticate postering decerebrate posturing
81
What are the alterations in arousal?
Metabolic: Alterations in delivery of oxygen ; seen with hypoxia, electrolyte disturbances, hypoglycemia Psychogenic: Uncommon, may signal psychiatric disorders, despite apparant unconsiousness ; person is physiologically awake
82
Evaluation of conscioussness
Level of consciousness Pattern of breathing Pupillary Reaction Oculomotor responses Motor responses
83
What criteria to be declared brain dead?
Irriversible cessation of all brain functions Asbcence of brainstem reflexes Coma Absence spontaneous Confirmed by: Physical assessment to confirm lack of responsiveness and brainstem reflexes EEG to monitor brain activity Apnea test to assess breathing without mechanical support
84
What's a persistant vegitative state?
Loss of higher brain functions but with preserved brainstem function Person may still be alive with basic reflexes and life support
85
Types of brain edema
Vasogenic: Caused by damage to blood vessels in brain allowing fluid to leak into brain tissue Cytotoxic: Caused by damage to brain cells, which then swell and accumulate fluid Interstitial: Caused by blockage of cerebrospinal fluid leading to accumulation in brain tissue Osmotic Edema: Caused by imbalance of electrolytes, causing fluid to move into brain tissue
86
Treatment of brain edema
Reduce ICP Manage underlying cause Remove excess fluids Correct electrolyte imbalanance
87
Stages of increased ICP
1: Normal 2: Episodes of confusion and restlessness Pupils still equal and reactive 3: Beginning of decompensation ; pupils small ; breathing slow
88
What do basilar skull fractures increase the risk of?
Infection of meningitis or brain resulting in leakage of CSF
89
What's a close brain injury ?
Head strikes surfaces Dura remains intact and brain is not exposed Coup: Directly below point of impact Contrecoup: Injury opposite side of impact Injuries include contusions, subdural or epidural hematomas
90
What's an open brain injury?
Injury breaks dura and exposes cranial contents of the environment Causes both faccal and diffuse injuries
91
What kind of hematomas are there?
Epidural Subdural Traumatic intracerebral hematoma
92
Epidural, subdrual, and traumatic intracerebral hematoma phases
Acute: Within 48 hours of injury theres symptoms Subacute: SYmptoms 2- 14 days after Chronic: symptoms weeks after
93
What's a subdural hematoma?
Bleeding between dura matter and arachnoid membrane
94
What's and epidural hematoma?
Bleeding between dura matter and skull Symptoms: Headache, vomitting, drowsiness, confusion, seizure
95
Acute subdural hematoma
SYmptoms worsen over time Homonymous hemianopia: Loss of vision in either right or left field , dysconjugate gaze, gaze palsies ; midline shift of greater than 5 mm are suggested as clinical parameters for surgery
96
Intracerebral hematomas
Bleeding within the brain Increases ICP Compresses brain tissue Causes edema
97
Whats a transient ischemic stroke?
Event lasting less than an hour
98
Thromolic stroke vs embolic
Thromolic: Thrombus formation in arteries supplying brain or intracranial vessels Embolic: Thrombus fragments obstruct brain vessels
99
What's cushing reflex?
Physiological respopnse to increased ICP Characterized by HTN, Bradycardia, Irregular Respirations ; indicates brain herniation

Pathophysiology (8 decks)

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