Exam 1 Blueprint Flashcards
Pathogenesis
How the disease or disorder develops.
Morphology
The shape and structure of components
Histology
Study of tissues and cells under the microscope
Clinical manifestations
How the disease presents, what signs and symptoms it causes.
Diagnosis
The determination of the nature of an illness or disease by examining the symptoms
Disease
A disorder of the structure or function of an organism that has a known cause and expected signs and symptoms.
Otitis Media
1. Common causes?
2. Risk factors?
3. How are children’s eustachian tubes different from adults?
Inflammation of the middle portion of the ear.
1. Can be caused by bacteria or viral pathogens
2. Smoking, daycare, bottle-feeding, feeding in the supine position, males, sharing a bedroom. The most crucial factor in development of OM is eustachian tube reflux. This connects the ear to the back of the throat which allows drainage and equalization of air pressure.
3. Children’s eustachian tubes are shorter, wider, and more horizontal. These factors can drastically increase the possibilities of OM development if a baby is primarily kept in the supine position.
How does OM typically present?
- Acute onset of otalgia (can be seen as pulling of the ear in infants)
- Fever
- Irritability
- Otorrhea
- Redness and inflammation when viewing the middle ear
Papilledema
The central retinal artery enters the eye through the optic papilla along with a vein. This is a small structure and during periods of increased intracranial pressure, this can reduce blood flow leaving through the papilla. This reduction results in vascular permeability and leakage of fluid resulting in papilledema.
The most common causes of this INCREASED ICP is DM, HTN, and cerebral tumors.
Allergic VS viral VS bacterial conjunctivitis
Conjunctivitis is the inflammation of the conjunctiva - AKA pink eye.
Allergic - typically characterized by itching and redness of the conjunctiva. Most common cause is season allergies.
Viral - adenoviruses, herpes, enteroviruses. Typically starts in one eye then spreads to the other.
Bacterial - can be hyper acute, acute, or chronic.
Hyper acute bacterial conjunctivitis is a sight threatening emergency caused by Neisseria gonorrhoeae or Neisseria meningitidis. This is especially dangerous in infants. Yellow-green drainage from the eye.
Acute presents with burning, tearing, and mucopurulent drainage.
What are the two mood disorders?
Depression and Bipolar
What is the neurophysiology behind mood disorders?
- Hypothalamus-pituitary gland-adrenal cortex axis hyperactivity. These structures work together to play a large role in neuroendocrine system. Higher cortisol levels.
2.Low levels of vitamin D - Early life stressors
- Familial aspect - genetics
- Elevated cytokine levels
Schizophrenia neurophysiology
- Dysfunction of neurotransmitters - dopamine, serotonin, and glutamate.
- Changes on imaging.
Alzheimer’s Disease
1. What is this disease?
2. What are the main features of the disease?
3. Diagnosis
4. Treatment
- Alzheimer’s Disease is a subset of dementia. It is a chronic neurodegenerative disease that results in loss of neurons in the cerebral cortex.
2A. Beta amyloid plaques build up in the cerebral cortex resulting in interference between neurons transmitting information.
2B. Neurofibrillary tangles - proteins used to keep neurons together are broken down. This results in clumping of the proteins called tangles.
2C. Both of these changes lead to apoptosis of some neurons resulting in loss of cortex. - Diagnosis of Alzheimer’s Disease can only be definitively done post-mortem via brain biopsy. Diagnosis made while living is via exclusion.
- No cure. Treatment is aimed at slowing down the progression and treating depression, sleep disturbances, and other factors that come with the disease. Cholinesterase is a medication that is used to slow the progression. It works by ensuring there are higher levels of Ach in the body. NMDA medications are used to affect glutamate
Guilian-Barre Syndrome
1. What is this disease?
2. How does this disease present? Progression? Time frame?
3. What symptoms are present?
4. Diagnosis?
5. Treatment?
- An acute inflammatory polyneuropathy. Typically follows gastroenteritis or URTI. Thought that antibodies mistakenly target myelin in the peripheral nervous system.
- GBS presents with a progressive symmetrical paralysis of the peripheral muscles leading proximally. The disease usually begins to improve (muscle paralysis returns proximal to distal, opposite of during the onset) in 2-4 weeks.
3A. Weakness - distal to proximal during onset, proximal to distal during improvement.
3B. Paranesthesia - numbness and tingling in the hands and feet.
3C. Pain - usually back of the legs
3D. Can affect the respiratory muscles requiring ventilation. Bulbar dysfunction.
3E. Can affect speech, making it slurred.
- Diagnosis includes EMG testing to look for the presence of peripheral neuropathy. Lumbar puncture looking at elevated protein levels with a normal cell count.
- Treatment - supportive care. IVIG treatments. Plasmapheresis.
Ischemic VS hemorrhagic strokes VS TIA
1. Describe these two processes
2. Describe the two mechanisms of ischemic stroke
3. What typically causes hemorrhagic strokes?
- Ischemic - blood flow is blocked from reaching a portion of the brain. More common. Ischemic strokes where symptoms resolve within 24 hours are known as transient ischemic attack (TIA).
- Hemorrhagic - an artery breaks inside the brain leading to a pool of blood that causes damage to the brain.
2A. Endothelial damage leads to atherosclerosis. These plaques pose the greatest risk if they become dislodged. Dislodged plaques are known as emboli and can travel throughout the vasculature until they become lodged blocking blood flow distal to their location. This causes the ischemic stroke.
2B. Thrombi are stationary blockages in the blood vessels that reduce blood flow distally. These are most commonly caused by atherosclerotic plaques that become uncovered. They quickly accumulate other material passing by leading to a large blockage of the vessel.
- HTN, arteriovenous malformations, secondary to ischemic stroke (hemorrhagic conversion).
What is a primary brain injury?
What is a secondary brain injury?
A primary brain injury is an injury to the brain that results when direct trauma occurs to the head and brain.
A secondary brain injury is an injury to the brain that occurs due to the physiologic processes that occur after a primary brain injury. Damage is done via brain swelling, cerebral hypoxia, or infection.
Hematomas
1. Types
2. Describe the presentation of an epidural hematoma patient.
3. Describe the presentation of a subdural hematoma patient.
Hematomas are a collection of blood in an enclosed space.
1. Brain hematomas include subdural, subarachnoid, epidural, and intracerebral.
- Epidural hematomas classic presentation is one of head injury involving fracturing of the temporal skull. This results in the rupture of an artery. The injury is followed by a brief period of unconsciousness followed by a period of lucidness which is then followed by a rapid progression to unconsciousness again.
- Subdural hematomas develop between the dura and the arachnoid space. This typically involves smaller veins in the area. The smaller vessels and the fact that they are venous instead of arterial leads to the potential for a slower, more chronic bleed.
3a. Acute subdural bleeds will present with symptoms within 48 hours of the injury. These present with a similar clinical picture as seen with epidural hematomas except without the lucid period. Highest mortality rate of any of the hematomas.
3b. Chronic subdural bleeds will present with symptoms as far out as two weeks post injury. Slow bleed is encapsulated by fibroblasts. Slowly grows in size causing changes in LOC, headaches, and mood alterations.
What part of the body does MS affect? How does it alter this part?
MS is a chronic demyelinating disease affecting the CNS. Results in loss of the myelin sheath (white matter). These sheaths play a pivotal role in the nervous system by protecting, nourishing, and speeding up neurons.
What signs and symptoms are seen with MS?
- Motor deficits: weakness, spasticity, tremors
- Sensory disturbance: paresthesia, hypoesthesia
- Bulbar dysfunction
- Vision disturbances
Common initial symptoms seen with MS patients?
An otherwise healthy patient presents with - paresthesia of the extremities, clouding of vision (optic neuritis), diplopia, or other types of gaze paralysis.
Describe the pathophysiology behind Myasthenia Gravis
What organ is often considered when discussing etiology?
MG is a result of autoimmune destruction of the Ach receptors located on the muscles side of the neuromuscular junction.
The thymus is often pointed to as a cause of this acquired autoimmune disorder.
Parkinson’s Disease
1. What is affected?
2. Presentation?
Parkinson’s disease is a disorder of the basal ganglia. Progressive destruction of the nigrostriatal pathway which results in decreased dopamine.
1. The basal ganglia - nigrostriatal pathway resulting in decreased dopamine. Dopamine is an important neurotransmitter in this pathway because it works to inhibit Ach - without adequate dopamine stores Ach results in impairment of the extrapyramidal tract.
2. Extrapyramidal tract alterations can be seen in tremors, muscle rigidity, bradykinesia, and changes in posture.
- Tremors - hallmark symptom
- Rigidity
- Bradykinesia - slow shuffling gait with body leaned forward to maintain center of gravity. Difficulty initiating movements or changes in directions.
What happens at the neuromuscular junction with MG?
MG is a disease that affects the peripheral nervous system, particularly at the neuromuscular junction. Autoimmune processes result in targeting of Ach receptors on the muscle side of the junction. This results in decreased ability to utilize Ach leading to fatiguability. Another form of the disease results in targeting of the Musk cells that help produce Ach. Decreased Ach also leads to the fatiguability that is classic of this disorder.
Fatigue, muscle weakness (eyes, resp, limbs, speech) are classic and worsen throughout the day as the stores of Ach are used up.
Pain Types
1. Acute
2. Chronic
3. Visceral
4. Cutaneous
5. Deep
6. Referred
- Acute - short duration. 6 months or less. Resolves when reason for pain resolves.
- Chronic - longer than 6 months. Sticks around even when the reason for the pain is gone.
- Visceral - deep pain. Common with disease processes.
- Cutaneous - superficial pain affecting the skin or close by structures.
- Deep
- Referred - pain felt in a location other than the area that was damaged. This is due to the referred site and the origin of pain sites sharing a dermatome
Innate immunity
This is the first line defense against invading microorganisms. The innate immunity barriers include the epithelium, mucus, leukocytes (macrophages, NK cells, DC cells, other phagocytic cells).
How to care for a patient anaphylaxis?
What are the problems being fixed?
Problems - the patient will experience inflammation as IgE antibodies cause a release of histamine. The patient can experience massive vasodilation as the body attempts to push blood to the inflammatory areas. If too much of the vasculature dilates, severe hypotension is seen. Laryngeal edema can cause ventilatory issues.
During anaphylaxis patients go into distributive shock. This results in loss of vascular tone, Steroids to reduce inflammation. Epinephrine to combat the massive vasodilation. It also relaxes the smooth muscle which line the airway.
Describe the process of anaphylaxis
1. What are common causes?
2. What cells are involved?
3. How does the first vs second differ?
4.
An allergen is introduced into the body. Common allergens include foods (peanuts, eggs, shellfish), medicines (penicillin), environmental (bee venom).
The allergen releases antigens into the body. The first cell to act on these antigens is the dendritic cells - they stimulate T-lymphocytes which stimulate lymphocytes to produce IgE. IgE bind to mast cells and basophils (two cell types that have granules). These cells release these granules as histamine which results in inflammation.
The second time this same allergen is introduced to the body, the body has already made proinflammatory molecules to respond to the allergen.
Primary VS Secondary immune response
Primary immune response occurs during the initial exposure to pathogens. The humoral immune system uses B-lymphocytes to create antibodies to respond to the invasion.
Pathogen is detected by APCs (DC, macrophages). These APCs take the antigen to MCH complexes. This information is then taken to CD4 helper cells which stimulate B-lymphocytes to create antibodies.
Secondary immune response occurs during the subsequent exposure to pathogens. The B-lymphocytes are quicker to mount their defense against the pathogen thanks to memory cells.
Active immunity VS Passive immunity
Active immunity - the host has to mount a immune response to invading organisms. Utilizes their innate and adaptive immune responses to mount a defense.
Passive immunity - the host is granted immunity from an outside source. The most common forms of passive immunity include that granted from mom to baby via the placenta and through breast milk. Immune infusions also grant limited passive immunity.
Epithelial Barriers and their role in immunity
The epithelium poses a large threat to invading pathogens.
1. Acidity of skin
2. epithelial cells are tightly packed together, leaving little to no room for invasion
3. Mucus membranes secrete mucus which immobilizes invading organisms allowing leukocytes to reach and deal with them sooner
4. Shedding of the skin
5. Keratin
How do the lungs affect acid-base balance?
The lungs affect A/B balance through increasing or decreasing the RR. A fast RR allows increased amount of CO2 to be expelled which has the effect of bringing up the pH (more alkaline). If the body’s a/b balance is too alkaline, then the body can slow the RR to keep more Co2 which lowers the pH level (more acidic).
How do the kidneys affect acid/base balance?
The kidneys can increase hydrogen excretion in cases where the bodies pH is too low (acidic). The kidneys can increase sodium bicarbonate reabsorption during times when the body’s pH is too low (acidic). Less H+ means less acidic. More bicarb means more alkaline. Both of these mechanisms work to combat acidosis.
What is edema? What different types are there? How is edema treated?
Edema is swelling of the body’s tissues. It more often occurs in dependent areas of the body.
Pitting edema - palpable edema. When pushed on will leave an indention.
Dependent edema - edema that is present in the body’s lower, dependent limbs.
3rd spacing - fluid accumulation in areas that are intracellular. This fluid is not readily avaliable to contribute to the vascular volume of the body.
Edema can be treated with non-pharm measures such as elevation, compression, movement, improvement of diet. Pharmaceutical measures include diruetics mainly.
Acute stress VS chronic stress
Acute stress activates the ANS resulting in the classic “fight or flight” response. This is a dilation of pupils to allow better vision, increased HR, BP, and RR to deal with suspected increased demands of the body during the stressful time. Blood is diverted from the resting organs to the more active organs during this time.
Chronic stress results in these same physiologic changes but they are detrimental. Because the body is exposed to these chemicals that cause the stress response on a consistent basis, the body builds a tolerance. This tolerance requires more and more of the chemicals to overcome which leads to higher and higher levels of effect. Chronic stress is linked to many different disease processes.
Marfan syndrome
1. Type of inheritance?
2. What does it affect?
3. How is this disorder treated?
An autosomal dominant disorder that affects the connective tissue in the body. The eyes, heart, blood vessels, and skeletal muscle are affected the greatest.
- Eyes - weakness of connective tissue can result in retinal detachment. Issues with the lens are common as well. Myopia.
- Heart - mitral valve prolapse, dilation of the aortic ring, and weakened aorta and blood vessels.
- Blood vessels - the connective tissue in the blood vessels is weaker which can lead to rupture or tearing in areas of high pressure like around the aorta.
- Skeletal muscle - typical changes include long thin fingers, kyphosis, scoliosis, long torso, chest deformities, long arms, joint hyperflexion.
Marfan syndrome is treated via supportive therapy. This includes echocardiograms to monitor the heart, ecgs, eye exams, and skeletal system monitoring.
X-linked recessive inheritance
This is a form of genetic inheritance that affects the sex chromosomes. Males are much more likely to be affected by x-linked recessive diseases due to the chromosol composition. Males have XY while females have XX. Because females have a second X chromosome to fall back on, they are protected from the recessive disorder from being expressed. Males on the other hand are likely to be affected because they only inherit one X.
Folic Acid deficiency
Folic acid deficiency is linked with birth defects. Folic acid plays an important role in the development of neural tubes. These tubes are the spine and other structures. They are developed early, often before the women knows she is pregnant. This is why it is recommended all females capable of becoming pregnant take folic acid supplements.
TORCH
A mnemonic that is useful in remembering what infectious diseases are commonly at the root of birth defects.
T - toxoplasmosis
O - other
R - rubella (German measles)
C - cytomegalovirus
H - Herpes
Period of vulnerability
This is a period of time where infants are at the greatest risk of becoming affected by teratogenic agents. This period of time is in the first 8 weeks of development.
Examples of primary, secondary, and tertiary prevention
- Primary prevention - education, immunization
- Secondary prevention - screenings, exercise, ASA to prevent MI and stroke
- Tertiary prevention - medications and procedures to slow the progression of the disease.
What foods are high in folic acid?
Green leafy vegetables, beans, lentils.
What is evidence-based practice?
Making scientifically based decisions supported by trails showing success.
Dystrophic calcifications Vs metastatic calcifications
Dystrophic - results when tissue is damaged, and the body starts to deposit calcium salts there despite a normal level of calcium in the blood.
Metastatic - results when tissue gets calcium deposits due to abnormally elevated blood calcium levels. These abnormal levels could be due to hyperparathyroidism, bone degeneration, tumors, CKD, etc.
