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158 Cards in this Set
- Front
- Back
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What is a seizure?
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sudden, explosive, disorderly discharge of cerebral neurons characterized by alterations in brain function
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What would you give a seizing adult?
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2 mg lorazepam/diazepam. Want to put the seizure out fast or it will be harder to stop
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What is the pathophysiology of a seizure?
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-Has a epileptogenic focus
-This group of neuronw develop a paroxysmal depolarization shift and sudden changes in resting potential -Neurons are hypersensitive and remain chronically partially depoloarized |
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What causes the tonic phase?
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firing of epileptogenic neurons increases in frequency and amplitude, reaching a threshold point of intensity, the excitation spreads through the brain and causes muscle contraction with excessive muscle tone
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What causes the clonic phase?
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The alternating contraction and relaxation of muscles occurs when inhibitory neurons in the brain begin to inhibit the excitation causing and interruption in the seizure discharge, producing an intermittent contract-relax pattern of muscle contractions. The bursts become less frequent until the epileptogenic neurons are exhausted and the neuronal membranes are hyperpolarized
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What is thought to be the primary abnormality in seizures?
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Neuron membrane defect resulting in instability of resting potential, abnormalities in K or Ca channels, defects in GABA inhibitory system, or defect in excitatory transmission enhancement
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What is the defect thought to cause generalized seizures?
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GABA inhibitory system
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What happens in a partial seizure?
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this only involves unilateral neurons, has a local (focal) onset. consciousness might be maintained if seizureis in one hemisphere (simple partial)
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What are the three types of partial seizures?
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simple, complex, secondarily generalized
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What happens in a generalized seizure?
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no local (focal) onset, involves neurons bilaterally, always involves imaired consciousness
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What are the types of generalized seizures?
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absence, tonic, clonic, tonic-clonic, atonic, lennox-gastaut syndrome
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What is epilepsy?
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recurrent, stereotypical, with the same seizure every time
-hypersynchronous neuronal discharges so the EEG looks normal -caused by lesion to brain, genetic componenet |
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What is the patho of epilepsy?
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has an epileptogenic focus where paroxysmal depolarization shift and sudden changes in resting potential.
-hypersensitive and chronically partially depolarized -tendency to depolarize -failure of inhibition -GABA inhibitory system |
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What happens in simple partial seizures?
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-no impaired consciousness
-with motor movements- usually these are clonic and body part affected depends on brain focus- usually hands and face, begins with jerking, stops spontaneously -if jacksonian march- seizure spreads to adjacent areas -if adversive- turning movement of hands and eyes to the side opposite of brain focus -if sensory- sensory experience during seizure |
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What happens in a complex partial seizure?
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-simple partial onset --> impaired consciousness
-cannot respond normally to exogenous stimuli, inappropriate movements -appears wide eyed might have automatisms- continue doing a complex activity such as driving -followed by postictal confusion |
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What happens in partial secondary generalized seizure?
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aura or partial onset --> generalized tonic-clonic seizure
-unconsciousness |
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what happens in an absence generalized seizure?
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Also called petit mal
-10 sec lapse in LOC -subtle clonic movements -if atypical might see lapses in LOC, changes in tone for 10-25 sec, awake with drowsiness and confusion |
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What happens in myoclonus and myoclonic generalized seizures?
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sudden uncontrollable jerking movements of one or more extremities or entire body, usually in am , no LOC, injury from jerking, may occur in clusters
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What does clonic mean?
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repetitive clonic jerks of constant amplitutde and diminishing frequency
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What does tonic mean? who does it affect?
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loss of postural tone, flexion of UE and extension of LE
affects children |
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What happens with tonic-clonic (grand mal) seizures? Who do these affect? What do you give for it?
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-usually aura and prodroma before
-sudden LOC, tonic clonic phases -lasts about 5 minutes -wake confused, HA, myalgia, fatigue |
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What happens in an atonic (drop attack)?
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sudden loss of postural muscle tone, tone loss may be mild or dramatic
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What is status epilepticus?
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experience of 2, 3, or more seizures before the person ahs regained LOC, or a single seizure lasting more than 30 minutes. Still in postictal state when the next seizure begins
-usually from abrupt d/c of seizure meds -may cause cerebral hypoxia, a med emergency -aspiration, mental retardation, dementia, other brain damage |
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Agnosia
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deffect in pattern recognition- a failure to recognize the form and nature of objects.
-involves a loss or recognition through one sense- might recognize with other sense -assocaited with CVA but might be from anything that injures that area of the brain |
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tactile agnosia
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inability to recognize objects by touch
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spatial agnosia r/t parietal lobe
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incapacity to find one's way around familiear places, disturbance of perception of space
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gertsman syndrome r/t left angular gyrus (parietal lobe)
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loss of spatial oreintation of fingers, body, sides, and numbers
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finger/digital agnosia r/t left angular gyrus (parietal lbe)
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inability to identify the names of ones fingers
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right-left confusion r/t left angular gyrus (parietal love)
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inability to distinguish right from left
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agraphia left angular gyrus (parietal lobe)
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inability to write
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acalculia
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inability to perform mathematic calculations
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visual agnosia
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1. object- inability to recognize objects and pictures
2. prosopagnosia- inability to recognize faces 3. color agnosia- inability to understand colors as qualities of objects |
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body name agnosias
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may be spatial
1. anosognosia- ignorance or denial of existence of the disease 2. autotopagnosia- loss of ability to identify the body, in whole or in part, or te recognize relationships among various parts |
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word blindeness
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alexia/dyslexia
inability to recognize written symbols |
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auditory agnosia
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pure word deafness, inability to recognize speech sounds
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amusia
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music deafness, loss of capacity to recognize tones and melodies
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aphasia
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loss of the comprehension or production of language
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dysphasia
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impairment of comprehension or production of language
-comphrension of use of symbols is disturbed or lost -usually with CVA in middle cerebral artery |
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expressive dysphasia
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expressive deficits, verbal comprehension deficit may be present
hard to find words, difficulty in writing |
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wernicke dysphasia
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fluent, able to produce language but it is meaningless, inappropriate words, etc.
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global receptive dysphasia
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-sensory, motor receptive, expressive
-nonfluent, produces little speech, at best speaks a few words or phrases |
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conduction receptive dysphasia
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fluent but with paraphrasia in self-initiated speech and writing or reading aloud
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anomic, nominal, amnesic
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fluent but impaired ability to name objects, persons, qualities, characterisitics, knows what he or she want to say but cannot find words, may even use desired word in another context but still cannot isolate word when needed
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transcortical motor dysphasia is...
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nonfluent
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transcortical sensory dysphasia is...
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fluent
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What is aphasia?
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loss of the comprehentsion or production of language
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What is Alzheimer's disease?
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a common neurologic disorder, a degenerative type of dementia
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What are the 3 types of alzheimers?
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late-onset familial
nonhereditary sporadic |
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What is the pathophys of alzheimers on the microscopic level?
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tau protein detaches from the microtubule and forms insoluble helical filaments or neurofirilllary tangles
-insoluble amyloid deposits in cerebral arteries causing amyloid angiopathy groups of nerve cessl, terminal axons, degenerate and coalesce around an amyloid core forming the senile plaques that disrupt nerve impulse transmission -increase plaques and tangles --> increase dysfunction |
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What is Alzheimer's disease thought to be related to?
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-loss of NT stimulation by choline acetyltransferase
-mutation for encoding amyloid precursor protien -alteration in apolipoprotein E -pathologic activation of NMDA which causes an excessive Ca influx |
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What is a neurofibrillary tangle?
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insoluble helical filament that is flame shaped
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How does aging/injury contribute to Alzheimer's?
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-decreased O2 and glucose transport
-loss of blood-brain barrier -mitochondiral defects that alter cell metabolism and processing of proteins including amyloid |
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What are S&S of Alzheimers?
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memory loss for recent events, moody, combative, lose ability to talk, walk, and eat
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How is Alzheimers dx?
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autopsy- atropy of gyri (folds) in cerebral cortex, neurofibrillary tangles and senile plaques (amyloid)
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Alzheimers has...
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degeneration of cholinergic neurons and deficiency of ACh and nerve growth factors
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What is meningitis?
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An infection of the meninges caused by bacteria, viruses, fungi, parasites, or other toxins. Can be acute, subacute, or chronic
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What is the pathophysiology of bacterial meningitis?
NOTE this is rare and most dangerous with 25% mortality |
Bacterial infection spreads to brain, primarily the pia mater, arachnoid, and subarachnoid space, ventricular system, & CSF. Bacteria multiply --> inflammatory rxn. Neutrophils migrate to SA space and interfere with CSF flow. If obstruct arachnoid villi --> hydrocephalus. Incraeased ICP may lead to secondary brain infection
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What is thought to be the entry route for bacteria into the brain?
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choroid plexus
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What are the clinical manifestations of bacterial meningitis?
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throbbing HA, photophobia, nuchal rigidity, Kernig and Brudzinzki signs, decreased LOC, palsies, seizures, tinnitus, vertigo
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What is the patho of viral (aseptic) meningitis?
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-inflamation believed to be limited to meninges, d/t virus or bacterial infection. Most often affects young adults
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What are the clinical manifestations of viral (aseptic) meningitis?
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mild compared to bacterial. Mild throbbing HA, mild photophobia, mild neck pain, stiffness, fever, malaise
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What is the patho of fungal (chronic)?
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Produce a granulomatous rxn with formations of granulomas ore gelatinous masses
-may extend into brain tissue causing infarction, hydrocephalu, and cranial nerve compression |
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What are the clinical manifestations of fungal meningitis?
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Develops insidiously over days or weeks. First manifestations are often dementia or communicating hydrocephalus
Typically afebrile |
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What is the patho of tubercular meningitis?
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Miliary tubercles form in the brain and meninges --> tuberculomas erode pia mater, mycobacteria enter CSF --> hypersenitivity rxn --> inflammation rxn
-Thistype is more common in AIDS |
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What are the symptoms of tubercular meningitis?
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HA, low grade fever, n/v, difficulty sleeping, fatigue, progresses to confusion, stiff neck, behavior change, seizures, hydrocephalus, CN palsies, cerebral infarcts
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What will you see in memingococcal meningitis?
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petechial or purpuric rash on skin & mucous membranes
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What are the symptoms of bacterial meningitis in the neonate?
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subtle, nonspecific, such as low grade fever, mild behavioral changes. may see high fever, lethargy, irritability, hpyothermia, incr ICP, vomiting, poor feeding
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How do you dx and treat bacterial meningitis in the neonate?
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CSF for dx
treat bact/fungal with ab aseptic with antivirals and steroids |
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What is cerebrovascular disease?
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any abnormality of the brain caused by a pathologic process in the blood vessels. This may lead to 2 types of CVA- ischmia (with or w/o infarction) or hemorrhage
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What is the cause of thrombotic CVA? describe what happens
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-Caused by thrombi formed in arteries supplying brain or in intracranial vesels (from atherosclerosis, increased coagulation, inadequate cerebral perfusion d/t dehydration, hypotension, etc)
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What are the clinical manifestations of viral (aseptic) meningitis?
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mild compared to bacterial. Mild throbbing HA, mild photophobia, mild neck pain, stiffness, fever, malaise
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What is the patho of fungal (chronic)?
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Produce a granulomatous rxn with formations of granulomas ore gelatinous masses
-may extend into brain tissue causing infarction, hydrocephalu, and cranial nerve compression |
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What are the clinical manifestations of fungal meningitis?
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Develops insidiously over days or weeks. First manifestations are often dementia or communicating hydrocephalus
Typically afebrile |
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What is the patho of tubercular meningitis?
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Miliary tubercles form in the brain and meninges --> tuberculomas erode pia mater, mycobacteria enter CSF --> hypersenitivity rxn --> inflammation rxn
-Thistype is more common in AIDS |
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What are the symptoms of tubercular meningitis?
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HA, low grade fever, n/v, difficulty sleeping, fatigue, progresses to confusion, stiff neck, behavior change, seizures, hydrocephalus, CN palsies, cerebral infarcts
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What will you see in memingococcal meningitis?
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petechial or purpuric rash on skin & mucous membranes
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What are the symptoms of bacterial meningitis in the neonate?
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subtle, nonspecific, such as low grade fever, mild behavioral changes. may see high fever, lethargy, irritability, hpyothermia, incr ICP, vomiting, poor feeding
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How do you dx and treat bacterial meningitis in the neonate?
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CSF for dx
treat bact/fungal with ab aseptic with antivirals and steroids |
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What is cerebrovascular disease?
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any abnormality of the brain caused by a pathologic process in the blood vessels. This may lead to 2 types of CVA- ischmia (with or w/o infarction) or hemorrhage
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What is the cause of thrombotic CVA? describe what happens
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-Caused by thrombi formed in arteries supplying brain or in intracranial vesels (from atherosclerosis, increased coagulation, inadequate cerebral perfusion d/t dehydration, hypotension, etc)
-may experience TIAs |
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What happens in an embolic stroke?
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Fragments that break from a thrombus formed outside the brain (in heart, aorta, carotid, etc). Associated with a-fib, MI, endocardidtis
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What happen in a hemmorhagic stroke?
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-Mass of blood is formed, volume increases --> displacement and compression of adjacent brain tissue, possible seepage into ventricles
-Due to HTN, ruptured aneurysms, vascular malformations, head trauma, tumor, anticoagulation, etc -Classified as massive, small, slit, petechial |
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What happens in lacunar stroke?
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-microinfarcts smaller than 1 cm, involveing small perforating arteries
-may have pure motor/sensory deficits -due to lipohyalinosis, subintimal lipid-loading foam cells, fibrinoid materelas that thicken arterial walls (smoking, HTN, DM) |
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What is a TIA?
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all neuro deficits clear within 24 hrs with no residual dysfunction, TEMPORARY
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What is guillain-barre syndrome?
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-Acquired inflammatory disease that results in demyelination of PERIPHERAL nerves with relative sparing of axons.
-Acute onset of motor paralysis, ascending -precipitating event: viral/bacterial infection -affects all ages and both sexes |
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What is multiple sclerosis?
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-dysimmune disorder involving degeneration of CNS myelin
-occurs when previous viral insult to nervous system has occurred in genetically susceptible individuals with an abnormal immune response in CNS --> plaques affect CNS white matter -precipitated by trauma, viral/bacterial infection |
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What happens in an embolic stroke?
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Fragments that break from a thrombus formed outside the brain (in heart, aorta, carotid, etc). Associated with a-fib, MI, endocardidtis
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What happen in a hemmorhagic stroke?
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-Mass of blood is formed, volume increases --> displacement and compression of adjacent brain tissue, possible seepage into ventricles
-Due to HTN, ruptured aneurysms, vascular malformations, head trauma, tumor, anticoagulation, etc -Classified as massive, small, slit, petechial |
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What happens in lacunar stroke?
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-microinfarcts smaller than 1 cm, involveing small perforating arteries
-may have pure motor/sensory deficits -due to lipohyalinosis, subintimal lipid-loading foam cells, fibrinoid materelas that thicken arterial walls (smoking, HTN, DM) |
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What is a TIA?
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all neuro deficits clear within 24 hrs with no residual dysfunction, TEMPORARY
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What is guillain-barre syndrome?
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-Acquired inflammatory disease that results in demyelination of PERIPHERAL nerves with relative sparing of axons.
-Acute onset of motor paralysis, ascending -precipitating event: viral/bacterial infection -affects all ages and both sexes |
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What is multiple sclerosis?
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-dysimmune disorder involving CNS demyelination
-Previous viral insult to NS has occurred in genetically susceptible person --> T-cells autoreact --> demyelinating lesions --> conduction block -Affects CNS white matter |
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What are the manifestations of MS?
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infection, trauma, optic signs and brain stem signs
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How do MS and guillian barre differ?
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MS- affects CNS, treat symptoms, cause is env, genetic, demyelination caused by lesions and plaque, progressive, relapsin, chronic, axon sparing
GB- affects peripheral nerves, caused by preceding illness, rehab, demyelination caused by inflammation, humoral and cell mediated immunity |
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What is anencephaly?
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-Soft bony compartment of skull and part of brain are missing
-frog-like appearance -die quickly |
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What is encehalocele?
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-herniation of protrusion of brain and meninges through a defect in the skull, most in occipital area
-surgical repair |
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What is a meningocele?
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-saclike cyst of meninges filled with spinal fluid when neural tube fails to close completely
-does not involve spinal cord |
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What is a myelomeningocele?
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-hernial protrusion of a saclike cyst containing meninges, spinal fluid and a portion of the spinal cord with its nerves
-one of the more common defects -hydrocephalus in 85% |
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What is cerebral palsy?
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group of non-progressive syndromes that affect the brain and cause motor dysfunction, classified by S/S into spasticity, ataxia, dyskinesia, or a mix
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What is the patho of CP?
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hypoxia and asphyxia --> edema of the brain
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What are some prentatal causes of CP?
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metabolic dx, nutritional deficeinces, multiples, bleeding, toxemia, exposure to radiation, infetion, PM labor, asphyxia --> cerebral hemorrhage, unknown, absence of corpus callosum, aqueductal stenosis, cerebellar hypoplasia
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What are some perinatal causes of CP?
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Anesthesia or analgesia during L&D, trauma during delivery, prematurity, metabolic, electrolyte
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What are some postnatal causes of CP?
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head trauma, infection, CVA, toxicosis, toxins
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What is Parkinsons disease?
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degenerative disorder of teh basal ganglia involving the dopamine secreting pathway
Primary- loss of pigmented neurons in the substantia nigra Secondary- caused by disorder other than Parkinson's |
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Name some sleep-provoked disorders?
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Intracranial P (REM), CAD (REM), bronchial asthma (REM), COPD (REM), uncontrolled DM (BG vary at night), duodenal ulcers (REM), brain attacks/stroke (Dreaming can increase HR)
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What is Reye's syndrome?
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Two phase illness (b/c of viral infection) that affects all organs of teh body, especially liver and brain
-an acute encepalopathy **Aspirin and salicylate increase risk** |
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What is the patho of Reye's?
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-viral infection (1 week before) and adpirin
-liver shows lipid deposids --> azotemia (urea in blood), brain is edematous -leads to hepatic failure, cerebral edema, death |
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What are the clinical manifestations of reye's?
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-Stage I- vomiting, lethargy, drowsiness
-Stage II- disorientation, delirium, aggressiveness and combativeness, central neurological hyperventilation, shallow breathing, hyperactive reflexes, stupor, convulsions, coma |
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What are migraine HA?
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benign recurring HA often provoked by a trigger factor and usually accompanied by neurologic dysfunction
-caused by regional hypoprofusion -phases: trigger, aura within inhibition of cortical activity and decreased blood flow, release of mediators, vasodilation |
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Migraine without aura
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common migraine, pain 4-72 hrs
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Migraine with aura
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classic migraine
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What is spina bifida?
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neural tube defect where the posterior vertebral laminae have failed to fuse w/o protrusion
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What is spina bifida occulta? what are some manifestations?
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no visible exposure of meninges or neural tissue
-tuft of hair on spine, midline dimple, port wine stain, subQ mass, usually no neurologic dysfunctions |
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What is dementia?
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a syndrome- progressive failure of many cerebral functions no caused by impaired LOC, biggest thing is to figure out if it is reversible
-culminates in nerve cell degeneration, brain atrophy involving the cerebral cortex, diencephalons and basal ganglia |
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What are schwann cells?
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specialized connective tissue cells in the PNS, form and maintains the myelin sheath --> membraine wrapped around the axons of neurons, nodes of ranvier form spaces on either side of the schwann cell
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What are oligodndroglia?
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form myelin sheath and meurolemma in CNS, much fewer than schwann cells
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What is autoregulation in the kidney?
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local mechanism that keeps the rate of blood flow and GFR fairly constant over time if the arterial blod pressure is between 80-180 mm Hg
-includes myogenic mechanism and tubuloglomerular feedback |
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Explain the myogenic mechanism of autoregulation in the kidney
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As arterial pressure decreases, the stretch on afferent arteriol decreases and arteriole relaxes to increase renal blood flow, and vice versa
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Eplain the tubuloglomerular feedback autoregulation in the kidney
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macula densa cells of distal tubule in JGA sense changes in flow rate and sodium content --> compensatory changes in afferent arteriolar resistance and GFR
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What does ADH do and where is it released from?
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-from posterior pituitary gland, triggered by hypothalamus when blood pressure drops
-increased water reabsorption by the ikidney by increasing water permeability of the distal tubule and collecting ducts -absence will cause large volume of dilute urine |
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What is renin?
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-stimulated by decreased BP in afferent arterioles, decreased sodium in distal convoluted tubule. Produced and stored by JGA
-Renin links with angiotensinogen --> AT I --> AT II --> aldosterone secreted by adrenal cortex, vasoconstriction, inhibits renin |
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What is aldosterone?
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boosts water reabsorption by kidneys by increasing NaCl resorption
- released from adrenal cortex, stimulated by angiotensin II |
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What is glomerular filtration rate (GFR)?
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-best measure of kidney function
-filtration of the plasma per unit time -related to perfusion pressure in glomerular capillaries -if <60 indicates kidney disease |
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What determines the severity of urinary tract obstruction?
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-location of blockage
-completeness of the blockage -involvement of one or both upper urinary tracts -duration -cause of the lesion |
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What is nephrotic syndrome?
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-excretion of 3.5g or more of protein in the urine per day
-Primary forms or idiopathic neprhotic syndrome with glomerular causes include membranous glomerulonephritis, focal and segmental glomerulosclerosis, and lipoid nephrosis -Secondary forms result from other organic pathological processes |
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Protein dumping is a characteristic of what?
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glomerular injury, hpoalbuminemia, edema, hyperlipidemia, and lipiduria
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What are teh clinical manifestations of nephrotic syndrome?
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edema, elevated plasma lipids, lipiduria, proteinuria, hyocalcemia, hyercoagulability
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How is creatinine produced by the body? Normal level?
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-biproduct of muscle metabolism
-When GFR is stable, creatinine has a constant rate of prouction- inversely related -useful to monitor progressive changes in chronic rather than acute renal disease b/c delays GFR by 7-10 days -can be increased by rapid muscle loss, trauma, surgery, etc -0.7-1.2 mg/dl |
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How is BUN produced by the body? Normal level/
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-Urea is formed in liver and is the end product of protein catabolism
-BUN increases as GFR drops, poor measure of GFR -might increase due to MI, GI bleed, fever, burns... -10-20 mg/dl |
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What is acute renal failure?
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An abrupt (within hours) reduction in renal function
-mostly reversible -BUN/creatinine increased -prerenal, intrarenal, or postrenal |
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What is prerenal acute renal failure?
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-caused by impaired renal blood flow, GFR declines due to decrease in filtration pressure
-might be from vasoconstriction, hypotension, hypovolemia, etc |
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What is intrarenal failure?
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-from ischemia (like after surgery) or nephrotoxic meds
-acute tubular necrosis is the most common cause |
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What is postrenal failure?
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-Rare, occurs with urinary tract obstruction that affects the kidneys
-commonly have hours of anuria with flank pain followed by polyuria |
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What are the clinical manifestations of acute renal failure?
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-oliguria
-increased BUN and creatinine -fluid retention --> edema -n/v -delayed wound healing |
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What is ischemic acute tubular necrosis?
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-most common cause of intrarenal acute renal failure
- most often after surgery due to hypovolemia -ischemia generates free radicals and inflammatory mediators that cause cell swelling, injury, and necrosis, a form or reperfusion injury |
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what is nephrotoxic acute tubular necrosis?
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-generally produced by antibiotics, especially aminoglycosides
-accumulate in renal cortex, may not cause problems until treatment is complete |
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What are the trhee pathophysiologic explanations proposed to account for the reduction of GFR and oliguria in acute renal failure?
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-back leak
-tubular obstruction -alteration in renal flow |
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What is the countercurrent exchange system?
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system in which fluid flows in opposite direction through parallel tubes, a concentration gradient causes fluid to be exchanged across parallel pathways
-longer the loop, greater the concentration gradient -loops of henle multiply the concentration gradient |
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What is the prevalence of renal calculi?
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2-3% with 50% recurrence in 10 years
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What are kidney stones? Risk factors? classification?
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masses of crystals, protein, or other substances that form within and may obstruct the urinary tract
-male, race, location, season, fluid intake, diet, occupation -classified by mineral comprising the stones |
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What are teh different types of kidney stones?
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-Calcium oxalate or calcium phosphate- associated with idiopathic calcium urolithiasis, 70-80% or renal calculi
-Struvite- 15%, contain magnesium, ammonium, and phosphate, associated with UTI by urease producing bacteria -uric acid- 7%, low urinary pH |
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What are the common organisms to cause UTI?
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-uncomplicated UTI- gram-negative bacteria like E coli, staph, enterobacter
-complicated-E coli -fungi |
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What is an uncomplicated UTI/
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otherwise healthy, might be isolated, recurring, or persistent
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What is complicated UTI?
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occurs in those with defects of the urinary system or other health problems
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What are risk factors for UTI?
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female, premature infants, sexually active women or using diaphragm/spermicide, DM, immunosuppressed, catheter, urinary obstruction
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How can you tell pyelonephritis from cystitis?
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Cystitis is inflammation of the bladder causing urinary frequency, dysuria, urgency or back/suprapubic pain
Pyelo is inflmattion of upper urinary tracts with flank pain Telling apart by symptoms is hard, look at lab tests and imaging |
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What is glomerulonephritis?
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inflammation of the glomerulus, often by group A strep, usually after strep infection. symptoms are hematuria, proteinuria, decreased GFR, oliguria, edema, HTN
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What portions of the kidney are affected by glomerulonephritis?
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glomerulus, glomerular membrane
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What is hypospadius?
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urethral meatus located on the ventral side of teh penis, caused by hormonal disruptions
-associated with chordee- shortage of skin on the ventral side of the penis |
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What is epispadias?
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-in males the urethra opens up on the upper penile surface
-in females, a cleft along the ventral urethra that usually extends to the bladder neck |
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What is bladder extrophy?
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lower urinary tract is exposed directly to the surface of the body with fissure in abdominal wall, due to failure to fuse in utero
-if unrepaired can lead to cancerous changes in 1 year |
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What is the relationship between the kidney and vitamin D?
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-When we take in vit D it is inactive and must be hydroxylated by liver and then kidney's to become active
-parathyroid hormone stimulated hydroxylation -prevented in renal failure |
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What is the relationship between the kidney and erythropoietin?
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- produced by kidney, stimulates the bone marrow to produce RBC in response to hypoxia
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What are the structures of the juxtaglomerular apparatus (JGA)?
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-juxtaglomerular cells- specialized cells around afferent arteriole where it enters renal corpuscle
-macula densa cells- portion of the distal convoluted tubule between afferent and efferent arterioles, senses sodium and chloride, change in flow rate, initiates changes in afferent arteriolar resistance and GFR -fxn- controls renal blood flow, GFR, renin secretion |
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What is nephrotic syndrome in children?
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-kidney is only or principal organ involved
-systemic or preexisting renal disease ro from other cause -secretion of 3.5g or more of protein in urine per day -will see proteinuria, hypoproteinemia, hyperlipidemia, edema |
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Qhat are the most common causes of idiopathic nephrotic syndrome in children?
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minimal change nephropathy and focal segmental glomerulosclerosis
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What is the first sign of nephrotic syndrome in children?
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-**periorbital edema**
weight gain, frothy/foamy urine, edema, protein deficiency, |
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What is Wilm's tumor?
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-nephroblastoma- embryonal tumor of the kidney from epigenetic and genetic changes
-most common solid tumore in childhoos, about 500/year in kids 1-5 -may occur in any part of kidney -have enlarging abdominal mass, asymptomatic |
