Pathophysiology
KU Patophysiology learning cards
KU Patophysiology learning cards
Fichier Détails
Cartes-fiches | 501 |
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Langue | English |
Catégorie | Médecine |
Niveau | Université |
Crée / Actualisé | 30.08.2022 / 27.12.2023 |
Lien de web |
https://card2brain.ch/box/20220830_pathophysiology
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What are the clinical manifestations of bladder cancer?
Painless hematuria (blood in urine), frequent and discomforting urination.
Bacterial infections can lead to obstruction and renal disease. Spreading of cancer can lead to death
What types of urinary tract infections are there and which ones are more serious?
upper and lower UTI's
The upper are more serious because they can cause renal damage
What is the etiology of UTI's?
People with urinary reflux, or disorders that impair bladder emptying, sexually active people, women, women in postmenopause, men with prostate disease, diabetes (suger in urine)
What is the patophysiology of UTI's?
Caused by bacteria, entered through urethra (or blood in immunocompromised people).
Distal portion of urethra usually contains pathogens, get washed out by urine though.
What are the clinical manifestations of Urinary tract infections?
Depends if upper (kidney) or lower (bladder) affected. Often frequent urination, pain while urinatin. Urine can be cloudy and foul smelling
What is Pyelonephritis?
Infection of the kidney parenchym (cortex and medulla) and pelvis. Can be acute (Upper UTI) or chronic (progressive process)
Describe Acte pyelonephritis
Upper UTI affecting cortex and medulla of kidney and renal pelvis. More common in people with diabetes and reduced immune response to infections.
Presents with chills, fever, nausea, vomitting, dysuria (pain when urinating), and abdominal pain
Describe chronic Pyelonephritis
Progressive procress, of scarring and deformation of renal calyces (cortex?) and pelvis due to bacterial infection, chronic obstructio or reflux. Can develop into acute pyelonephritis
Loose functio to concentrate urine, polyuria, nocturia, hypertension, fever, nausea, vomitting, abdominal pain
Explain briefly what a stroke is?
Poor blood flow to the brain due to a vascular disorder. Result in injury of brain tissues
What is the etiology for stroke?
Risk factors are age, sex (higer in males), family history, cardiac disease, previous histories of stroke, blood disorders, hypertension, diabetes mellitus, smoking, or hypercoagulopathy.Atrial fibrilation froms blood cloths and thus also risk factor.
Obesity, physical inactivity, oral contraceptive, hormone replacement therapy, alcohol and drugs
What two types of strokes are there? explain
Ischemic stroke: caused by cerebrovascular obstruction (thrombosis or emboli)
Transient Ischemic attack (TIAs): temporal disturbance of cerebral blood flow that reverses before infarction occurs
Hemorrhagic stroke: Most frequent and fatal. Rupture of cerebral blood vessel -> edema
Explain what a Anaurysmal Subarachnoid Hemorrage is?
Hemorrhagic stroke caused by cerebral aneurysm which leads to bleeding in subarachnoid space
What are the clinical manifestations of a cerebral aneurysm?
Before rupture/bleeding: Asymptomatic, headaches, nausea, vomitting and dizziness.
After: Same as before, If severe bleeding, collaps and loss of consciousness. neck stiffness, motor and sensory deficits
What are the clinical manifestations of a stroke?
Determined by the artery affected/area of brain without O2. Symptoms often sudden and one-sided!
facial droop, arm weakness, slurred speach, imbalance, Language deficits, sensation and cognition deficites.
Spasticity due to increased muscle tone
Explain epilepsia briefly
Abnormal discharge of neurons. Can occure during all serious illnesses that affect the brain and metabolism of it (tumor, infections, drug abuse,...)
Seizure is a single event, epilipsy is a chronic disorder
What is the etiology of epilepsy?
Birth injury, or congenital malformation.
Head trauma, drugs, stroke or tumor can cause it
What is the patophysiology for Epilepsia?
Abnormal, and excess excitation of some cortical neurons (due to altered membrane permeability or distribution of ions)
What classes of seizures are there?
Focal seizure (specific area of brain): With or without impaired awareness. (without: no symptoms or movement when motor area involved. With: Confusion, hallucinations, Illusions, lip smacking, grimacing,..)
Generalised seizures (simultaneusly in both hemispheres): Motor (contraction of muscles with loss of awareness) or non-motor (brief loss of contact with environment)
Non-epileptic seizures and status epilepticus (does not stop spontaneously -> can lead to death because respiratory failure ect.)
Name a few clinical manifestations of epilipsia
Impaired motor function or loss of awareness (depends on type of seizure)
Explain headaches briefly. What types are there?
Can be primary or secondary to other disease, like meningitsi, brain tumor, cerebral aneurysm, hemorrage,...
Migraine headache: tends to run in families
Cluster headache: occurs frequently in a month then not (in clusters)
Tension-type headache: most common type
What is the etiology and patophysiology of migraine headaches?
Runs in families, may be inherited. Hormonal variations play a level (woman) but also dietary substances
Patophysiology is not fully understood. Neurogenic inflammation
What is the clinical manifestation of Migraine?
Without aura: Pulsating, thorbbing, lasts 1-2 days, more serious with physical ativity, nausea, vomiting, sensitivity to light
With aura: Additionally reversible visual, sensory symptoms or speech disturbances (develops over few minutes and lasts up to 1h)
Explain the etiology and pathogenesis of cluster headaches
More frequent in men. Most uncommon type of headache.
Patophysiology not fully understood. Interplay of vascular, neurogenic, metabolic and hormonal factors and or autosomal dominant gene.
What are the clinical manifestations of cluster headaches?
Rapid onset pain, peaks in 10-15 min. Pain behind eye, restlesness, tears on one side, eyelid edema, swating on forhead and face
What is the etiology and pathogenesis of tension-type headache?
Most common type, usually not severe enough to interfere with daily activities.
Mechanism is unknown. May result from sustained tension of mscles (neck, scalp) or migraines that slowly transform to chronic. Also caused by stress, anxiety and depression, caffein overuse
What are the clinical manifestations of tension type headache?
Dull, aching, diffuse headaches, around the head. NOT associated with nausea, vomitting or worsening with physical acitivity
What are CDH? Etiology and pathogenesis?
Chronic Daily Headache (CDH)
Cause is unknown, but hypothesis assumes transformed migraine, or posttraumatic headaches. Sometimes related to medication overuse
What are the clinical manifestations of CHD?
Certain characteristics of migraine, others resemble chronic tension type headaches.
Explain Pain in children
Responsiveness to painful stimuly begins in newborn period. Pain response evolves with maturation and cognitive development. Neurons in neonates have wider receptive field and lower treshold
Explain pain in Adults
Frequently underrecognized and underrated. Williness to report differs with age.
Difficulty locating pain and assess intensity
What is the etiology of pain?
Usually in contex with injury or inflammation. Can be chamical (tissue trauma or ischemia) thermal, mechanical
What is the patophysiology of Pain?
Tissue injury leads to release of inflammatory mediators. Nocirepors respond to chemical, thermal, mechanical changes and Thalamus stimulates hypothalamus (endocrine response), emotional experience (limbic cortex) and locatio of intesity and location.
What types of Pain are there?
Acute pain: duration <6 months, Increased autonomic response (Hear rate, Blood Pressure, muscle tension,..). associated with anxiety
Chronic pain duration >6 months, absence of autonomic response but increased irritability, depression, loss of appetite, sleep disorders
Deep somatic pain: Strong pressure on bone, muscle ischemia, dissue damage
Referred pain: Pain in different site than original (e.g Myocardial infarct)
Visceral pain: Commonly produced by diseases. Contractions, ischemia of visceral wall
What is the etiology of Parkisons disease?
Age (onset usually at around 56 years).
Believed to be caused by interaction of environmental and genetic factors. Oxidative stress and mitochondrial disorders.
Contact with pesticides, or rural living increases (while coffe and smoking lowers) risk.
What is the patophysiology of Parkinsons disease?
Degenerative disorder of basal ganglia function. Destroys nigrostriatal pathways progressively and reduces striatal dopamine. Some residual neurons are atrophic, few contain Lewy bodies (spherical eosinophilic inclusions)
What are the clinical manifestations of Parkinsons disease?
Loss of dopamine nerve cells, leads to:
Tremor (Involuntary oscilating contractions of hands, feet, neck, tongue, jaw) resembles movement of rolling pill between fingers.
Rigidity: resistance to full range of movement -> leads to jerks/ratchet-like movements
Bradykinesia: Slowness in initiating and performing movements. People freeze in place when walking, higher risk to fall, loss of blinking reflex, tongue and throat muscles become rigid -> speed becomes slow....
What is Amyotrophic Lateral Sclerosis and it's etiology?
Neurological disorder that selectively affects motor function (upper motor neuron disease).
People in their 50s, Males and with family history
What is the Pathophysiology of ALS?
Affects the lower motor neurons of the spinal cord and upper motor neurons of the cerebral cortex. Undergo degeneration of distal terminals until cell dies. Sensory system remains intact.
Can be caused by gene mutation or a suggested exotoxic injury. Autoimmunity has also be suggested
What are the clinical manifestations of ALS?
Due to UMN or LMN (lower motor neurons) involvement:
UMN: weakness, stiffness, impaired fine motor control
LMN: weakness, muscle fiber atrophy, muscle cramps
Speech, chewing, swallowing is impaired because muscles are involved. No cure for ALS, results in death (respiratory muscles)
What is MS, explain briefly
Multiple Sclerosis
Inflammation and destruction of the CNS myelin (PNS usually spared)