Patho final Flashcards
Multiple Sclerosis
- 20-50 yrs old
- Chronic demyelination of CNS that results
in scarring - 4 different types
1) remitting-relapsing
2) primary progressive
3) secondary-progressive
4) progressive-relapsing - Causes
1) Autoimmune - prior virus infection, genetic, environment-away from equator
2) FHx? 15% of MS pts have a family member with MS
Identical twins - 30% chance of getting MS
3) F>M - Signs and Symptoms – vary due to which nerves are affected
1) Need 2 separate episodes at different locations to help diagnose
2) Visual changes – unilateral acute, due to cranial nerve demyelination- Optic neuritis
3) Balance, memory, weakness, fatigue, spasticity, bladder dysfunction
4) Tremor, lack of coordination or unsteady gait
- Optic neuritis
- 4 different types which really means four different ways the disease can progress
- Know these causes
- Correlation with prior virus not causation
- Tightest correlation is family history
- Females statistically get it more than guys
- Two separate episodes at two different locations in the body in order to have MS
Multiple Sclerosis nerves
The nerves that branch off the central nervous system (CNS) provide messages to the muscles and organs for normal function. When there is CNS damage, the function of these organs and tissues may be compromised. In multiple sclerosis, the demyelination of nerve cells may lead to bowel incontinence, bladder problems and/or sexual dysfunction.
Multiple Sclerosis testing
- Testing – hard to diagnosis-process of elimination
- MRI
- Demyelinating lesions in white matter - sclerotic plaques (gliosis) are diagnostic
- Lumbar puncture – specific pattern of antibodies
- Oligoclonal bands (IgG) – 90% of MS pts
- Evoked Potential tests
- Nerve conduction speed
- Can sometimes see demylination on the MRI
- Oligo means having few, not a lot of
Multiple Sclerosis oligoclonal bands
- Each of the two to five oligoclonal bands seen by protein electrophoresis represent proteins (or protein fragments) secreted byplasma cells into the CSF, although why exactly these bands are present, and whichproteinsthese bands represent, has not yet been elucidated. Approximately 79%-90% of all patients with multiple sclerosis have permanently observable oligoclonal bands.
- IgG oligoclonal bands (OCBs) represent IgG unique to the cerebrospinal fluid (CSF), that is, without corresponding IgG in the serum. They are commonly used as part of the diagnostic workup for multiple sclerosis (MS) but are not essential to make the diagnosis. OCBs are not unique to MS; rather they provide evidence of IgG synthesis thought to reflect the compartmentalized central nervous system (CNS) humoral immune activation present in MS. OCBs are found in other inflammatory and infectious diseases affecting the CNS, although these can be differentiated from MS using additional CSF and/or clinical findings.
- The bands tend to disappear from the cerebrospinal fluid as a person recovers from the neurological disease.
- Not diagnostic but can help lead to proper diagnosis
Multiple Sclerosis main points
- Autoimmune
- Usually females
- family history
- Tinnitus
- Decrease hearing
- Nystagmus
- Diplopia
- Blurred vision
- Dysarthria
- Dysphagia
- Onset 20’s to 40’s
- Urinary retention
- Spastic bladder
- constipation
- Weakness may progress to paralysis
- Muscles spasticity
- Ataxia
- Vertigo
ALS - Amyotrophic Lateral Sclerosis
- Atrophy of upper AND lower motor neurons
- Lou Gehrig disease
- Causes
- Idiopathic, M>F, 40-60
- Genetic > possibly multifactorial
- Possibly excess glutamate
- Signs and Symptoms
- Diminished muscle strength progresses to atrophy
- Weakness and spasms, difficulty speech, fatigue
- Spastic & flaccid paralysis (depending on severity of UMN/LMN lesion)
- Respiratory infections
- No intellectual or sensory impact
- Testing
- MRI
- Nerve and muscle conduction tests
- Increased GLUTAMATE (neurotransmitter that is usually quickly cleared)
- Has a toxic effect on nerve cells
- Tx - riluzole (Rilutek) – extends time. No cure (average 3 – 5 years post Dx)
- Riluzole is a neuroprotective drug that blocks glutamatergic neurotransmission in the CNS. Riluzole inhibits the release of glutamic acid from cultured neurons, from brain slices, and from corticostriatal neurons in vivo. Riluzole also blocks some of the postsynaptic receptors for glutamic acid.
- Damage to both upper and lower motor neurons (brain and spinal cord)
- Idiopathic (just don’t know)
- Upper and lower motor neuron signs
- They think just fine
- Only treatment on the market is riluzole (rilutek) blocks release and binding to post synaptic
ALS - Amyotrophic Lateral Sclerosis little points
- Could be in brain stem or spinal nerves
- Cranial nerves are lower motor neurons
- Possible cause too much glutamade
Parkinson Disease
- Movement disorder
- Causes
- Lack of dopamine
- Signs and Symptoms
- Insidious onset
- Resting tremor, pill rolling, bradykinesia, wide gait, loss of facial expressions
- Later stages - dementia
- Testing
- CT
- R/O other neurological disorders
Parkinson Disease – Levadopa Tx
Levodopa is converted to dopamine via the action of a naturally occurring enzyme called DOPA decarboxylase. This occurs both in the peripheral circulation and in the central nervous system after levodopa has crossed the blood brain barrier. Activation of central dopamine receptors improves the symptoms of Parkinson’s disease; however, activation of peripheral dopamine receptors causes nausea and vomiting. For this reason levodopa is usually administered in combination with a DOPA decarboxylase inhibitor (DDCI), in this case carbidopa, which is very polar (and charged at physiologic pH) and cannot cross the blood brain barrier, however prevents peripheral conversion of levodopa to dopamine and thereby reduces the unwanted peripheral side effects of levodopa. Use of carbidopa also increases the quantity of levodopa in the bloodstream that is available to enter the brain.
Strep throat
Post strep glomerulonephritis (if left untreated in kids), commonly effects children, red or cola-colored urine, hypertension, decrease in GFR
Links - Rheumatic fever
Treatment - Antibiotic therapy, control the symptoms so it doesn’t lead to kidney failure & high BP
Myocardial Infarction
AKA “Heart Attack”
Progressive ischemia with damage to myocardium (myocyte necrosis)
2 types
Subendocardial MI
Thrombus dislodges and only myocardium directly beneath endocardium involved
Transmural MI
Thrombus remains and myocardium involved transcends to epicardium
Myocardial Infarction s/s
S/S: Dyspnea Sudden severe chest pain with radiation Nausea/Vomiting Anxiety/dizzy/cough Diaphoresis – profuse sweating Heart Attack Video Clip Causes: Cardiovascular disease – what are the risk factors?
Myocardial Infarction tx
Angioplasty Animation Video Clip
Real Angioplasty (Video Clip)
Thrombolytic therapy – w/in 3 hours
Cardioprotection after MI:
Beta-blockers – blocks sympathetic innervation
ACE inhibitors – How does this work? – next slide
Female heart attack symptoms
- n/v
- jaw pain
- back pain
Myocardial Infarction tests
Tests:
- EKG
STEMI – indicates transmural MI
non-STEMI – indicates subendocardial MI
-Tests: BP – Initially decreases SNS reflexively activates Temporarily increases HR and BP Abnormal extra heart sounds – LV dysfunction Pulmonary congestion Dull percussion Inspiratory crackles at lung bases
-Tests: Blood test values increased Troponin I & T – lasts 1 week (most specific) LDH – Lactic dehydrogenase CK-MB – Creatine kinase-myocardial bound Lasts 48 hours Less specific May be elevated in COPD, 3rd degree burns Myoglobin – lasts 24 hours Not specific for cardiac muscle
Myocardial Infarction s/s
Dyspnea, chest pain w/ radiations, N/V, Anxiety, diaphoresis
Hodgkin’s Lymphoma
B cell lymphoma High cure rate: 5 year survival rate: 83% Causes Most common in young adults 2 peaks: 30-40 & 60-70 FHx, Epstein-Barr Virus Signs and Symptoms Painless lymphadenopathy All other leukemia S/S discussed Reed-Sternberg cells Testing
- Good cure rate
Find this in young adults
Start a list of diseases that the epstein barr virus pops up in this class
Family history is big in this disease
Painless lymphadenopathy=disease of the lymph node, if the lymph node hurts and you can move it around under the skin you are generally good if they don’t hurt and if they are fixated that’s bad
A normal lymphocyte is noramally all nucleus with this disease you get reed sternberg cells that look like owl eyes
Multiple Myeloma
- Plasma cell neoplasm > involvement of the skeleton at different sites
- Causes
- Idiopathic
- Possible chromosome 13 deletion (50% of cases)
- Link to infection by Human Herpes Virus 8 (HHV-8)
- Kaposi’s sarcoma – HHV-8
- Signs and Symptoms
- Incidence > men
- Peak age 50-60
- Suppression humoral immunity > recurrent infections
- Why is the humoral immunity suppressed?
- Anemia
- Hypercalcemia – confusion, weakness, lethargy, constipation, punched out lesions > pathological fractures
- In multiple myeloma patients, the primary cause of the hypercalcemia is widespread tumor-induced bone destruction. This is primarily due to increased osteoclastic bone resorption caused by potent cytokines expressed or secreted locally by the myeloma cells (receptor activator of nuclear factor-κB ligand [RANKL], macrophage inflammatory protein [MIP]-1α, and tumor necrosis factors [TNFs]
- Plasma cells make antibodies
This cancers spues out antibodies but not normal functioning antibodies
Usually older guys get this
Can get anemia with this
Big clue on exam: person could be hypercalcemia, if you do an x ray you would see bone loss/absorption/breakdown
RANKL stimulates osteoclast activity which breaks down bone tissue
2 proteins that these cancerous plasma cells make
The full antibody is call m protein the light one is called jones something?
Hypercalcemia might lead to nephr
Multiple Myeloma
- M-protein
- Most prominent protein in the blood - monoclonal proliferation of plasma cells in the bone marrow, meaning that there are a high number of malignant plasma cells that all originated from the same initial cell - secreting exactly the same form of immunoglobulin
- Due to large number of malignant plasma cells
- Bence Jones protein (80% of cases)
- Frequently found
- Immunoglobulin light chain found in blood and urine
- Contributes to damage of renal tubular cells
- PUNCHED OUT LESIONS on X-RAY
Polycythemia Vera (1 in 200,000 in US)
- Abnormal, slow, idiopathic proliferation of RBC at bone marrow (WBC and platelet counts may also be elevated) increased risk for AML later in life
- Primary polycythemia - neoplastic proliferation and maturation of erythroid, megakaryocytic and granulocytic elements to produce what is referred to as a panmyelosis
- Secondary polycythemias - low serum level erythropoietin (EPO). PCV cells have a mutation in the EPO receptor, which makes them hypersensitive to EPO
- S/S: due to increased blood volume & hyperviscosity
- Splenomegaly, thrombi, HA, tinnitus, chorea, delirium,
- Visual disturbances, angina, thrombosis, ischemia, infarct
- Pruitis after warm bath/shower
- Plethora (ruddy complexion) in the face, palms, nail beds, mucosa, and conjunctiva.
- Testing: CBC
- Tx:
- Meds for bone marrow suppression
- Phlebotomy
- Low dose aspirin
- Poly means multiple cyt means cell emia means blood so a lot of red blood cells
- Two main types: primary vs. secondary
- Neoplastic is new growth
- Primary is a pan (everything) increase in all of the blood cell types
Polycythemia Vera
Polycythemia is a condition of increased production of red blood cells (RBCs). The percentage of RBCs in the blood may become so high that the blood ceases to flow in some smaller vessels and capillaries. In this photomicrograph, the RBCs are densely packed together.
Hirschsprung’s Disease– Congenital Megacolon
- Causes
- Missing intestinal/rectal ganglion cells
- Malformation of the Parasympathetic NS (80% rectal end)
- Inherited?
- Main cause of colon obstruction (infants)
- Missing intestinal/rectal ganglion cells
- Signs and Symptoms
- Delayed meconium stool at birth
- Vomiting, colic, distended abdomen (gives the name megacolon), “ribbon-like stool”
- Toxic- enterocolitis > life threatening, fever, swollen abdomen, explosive and bloody diarrhea
- Testing
- Anorectal manometry
- tests sphincter muscle strength and nerve supply
- CT/X-Ray
- Rectal Biopsy
- Anorectal manometry
- Ganglia in parasympathetic are located far away from the spinal cord
- Sympathetic and parasympathetic is a two neuron system to get to the target neuron
- In this case the target organ is the colon
- They don’t have ganglia cells in congenital megacolon
- They are missing ability to produce para something waves
- If fecal material can’t move it builds up so the colon enlarges proximal, before, the area that is missing the ganglia
- Toxic entercolitis is bad it is a build-up of fecal matter in the colon
anorectal manometry they put a ballon into rectal area - When rectum stretches due to fecal matter the spincter SHOULD relax
Hirschsprung’s Disease– Congenital Megacolon
Dilation of bowel (megacolon) proximal to the affected region of narrowing at the lower left center in sigmoid colon. Mucosal damage and secondary infection may follow.
Hirschsprung’s Disease– Congenital Megacolon
A barium enema showing a “long segment” Hirschsprung’s disease. The transition zone is in the large intestine in an area going across the abdomen called the transverse colon. The arrow demonstrates the area of the transition zone between the enlarged area which has ganglion cells (normal) and the small area which does not (Hirschsprung’s disease).
- When patient swallows Barium you will be able to see the dilated bowel
Everything proximal to it is full, it can’t move
Side note: review autonomic nervous system: parasympathetic and sympathetic
Polycystic Ovarian Syndrome (PCOS)
- 1 out of 15 women: main cause of hormonal disease of women at childbearing age
- Causes
- Genetic
- Unknown: Hormonal imbalance
- Increased insulin (due to resistance) causes increase in androgen (male sex hormone) production?
- Signs and Symptoms
- Ovaries with multiple cysts
- increase LH secretion > increase Androgens (T, androstenedione, DHEA) > increase conversion to Estrogen without enough Progesterone to balance > endometrial hyperplasia > risk endometrial CA
Irregular or absent menses (due to high estrogen exerting negative feedback on FSH)
– Infertility Virilization – females gain male traits (inc body hair distribution) - Obesity (41% are obeses)
- Insulin resistant (prediabetes or DM type 2) (can lead to type 2 diabetes)
- Acanthosis nigricans – a result of having insulin resistance (this is the photo, the darkening of the skin)
- Higher incidence of
- HTN
- Hyperlipidemia
- Nonalcoholic Steatohepatitis (NASH)
- Fatty liver
- Elevated CRP > CV risks
- Testing
- Hormones
- US/CT
- R/O sources of hormone secretion
- TX: No cure, treat the symptoms
- Very common
- Differs from one female to another
- Hormonal imbalances is a huge cause
- There is a correlation but not a causation with increased insulin
- The male sex hormones are converted to estrogen which is a normal process.
- The longer a women is exposed to estrogen the higher the risk for developing endometrial cancer.
Polycystic Ovarian Syndrome (PCOS)
- LH is abnormally high and stays high this goes to theca cells in the ovary which make androgens (male sex hormones) this can lead to hirsutism (excess hair)
- Normally excess androgens should loop back and do a negative feedback but with this disease it stays high and FSH is low. Normally FSH tells the granulosa to mature but with this disease there is no egg release. (that is why it can lead to infertility)
Wilm’s Tumor (rare) 1 in 10,000 children
- Mixed tumor of the kidney in children
- Causes
- Unknown
- Chromosome #11
- Mutation
- Inherited
- S/S
- less than 5 years old, peak age 2-3 years old
18% will show other congenital abnormalities
Lacking of iris: Aniridia (genes for eye formation also on Chromosome 11)
Asymptomatic upper abdominal mass
Hypertension due to tumor secreting Renin
Parent feels an abdominal mass when bathing child
Testing
Abdominal U/S, CT, MRI, Surgical biopsy
Treatment: Surgery with radiation therapy post-op
- less than 5 years old, peak age 2-3 years old
- Rare, look for in a younger individual it might pop up in a kid 2-3 years old
Huge tumor in the kidneys
Classic board NCLEX Q is: aniridia is without much of an iris. It is the photo of the eye. What else might you see in this individual? Hypertensive, parent feels abdominal mass when bathing child,
Renin increases BP
Lung cancer
- Leading cause of death in US
- Smoking (85%)
- Small cell carcinoma/ Oat cell carcinoma (CA cells are small)
- Smokers
- SIADH (too much ADH), ectopic ACTH (paraneoplastic syndromes resulting from tumor-produced substances)
- Non-small cell carcinoma
- Smoking, Second-hand smoke exposure, metastasis, toxins (asbestos)
- Adeonocarcinoma
- Signs and Symptoms
- Dyspnea, SOB, hemoptysis, persistent cough or changes in chronic/smokers cough
Psoriasis
Causes
Autoimmune T-cell reaction to skin
Risk factors:
FHx, genetic predisposition, HIV, stress, obesity, smoking
Triggers: Alcohol, stress, infections, injury to skin, cold weather, certain meds (Lithium – for bipolar disorder)
Main areas: Elbows, knees and scalp
Signs and Symptoms
Red skin with silvery scales and inflammation
Nail involvement: pitting, onycholysis
Separation of nail plate
Psoriatic arthritis-skin disease precedes in 80%
Testing
Clinical
R/O RA
Nephrolithiasis
Kidney Stones
Calcium Oxalate, Struvite (Mg)
Uric Acid
Causes
M 12%>F 5% (30-50% get a second one) and age
Dehydration
Abnormal Calcium metabolism
Hypercalciuria –hyperabsorption of dietary calcium
Prolonged immobiliazation – bone demineralization
S/S
Flank (Renal colic) or Abdominal pain
N/V, Dysuria, Hematuria,
Testing
UA, CT now, used to be IVP (Intravenous pyelogram)
an X-ray of the abdomen along with the administration of contrast dye into the bloodstream
Renal Function BUN, Creatinine (by-product muscle metabolism), Uremia
Calcium: Parathyroid Hormone
Right Heart Failure
Inability of right side to adequately pump venous blood into pulmonary circulation
1) Left ventricle output exceeds right ventricular output
2) Pressure backs up
3) Fluid accumulates in systemic tissue
SIADH Syndrome Of Inappropriate ADH Secretion
- Excessive secretion of ADH
- Causes
- Idiopathic
- Brain injury, infection, trauma, stroke, hemorrhage
- ADH secreting tumor (bronchogenic cancer *most common)
- Signs and Symptoms
- Hyponatremia (does this make sense?)
- Dilutional hyponatremia from water intoxication
- Testing
- ↓Serum osmolarity vs.↑Urine osmolarity
- Too much TBW should lead to more urine, right?
- The low serum osmolarity suppresses Renin
and Aldosterone so Na+ is not reabsorbed. More concentrated urine results - CT/MRI – tumor?
Potassium (K+)
3.5-5.0 mEq/L (ECF) Major cation inside of cell (95-98%) Function Maintains ICF osmotic balance Glycogen/glucose deposition Liver and skeletal muscle Transmission of nerve impulses Maintenance of normal cardiac rhythms, skeletal and smooth muscle contractions - Organs and Hormones involved 1) Kidney 2) Aldosterone
- Memorize this
Know: maintains intracellular fluid osmotic balance, clinically important: glycogen/glucose depostiion (liver/skeletal muscle)
What hormone drives sugar into a cell? Insulin, it also helps to drive potassium into the cell.
K is important for normal resting membrane potential and action potentials
Important for heart rate, especially the pace maker of the heart
Kidney is major organ that gets rid of or hangs onto it
Potassium function
The greatest contributor to intracellular osmosis and cell volume
Determines the resting membrane potential of a cell
Plays a role in blood pH by affecting the plasma concentration of H+
Determine what happens to the resting membrane potential if extracellular potassium rises
Determine what happens to extracellular potassium levels if blood pH drops
-Potassium holds water inside of a cell. Also important for keeping proton concentration in blood where it should be.
If someone is acidosis that is talking about the blood: low pH protons are causeing this protons makes it more acidic
Kidneys can acidify the urine
Can also sort of breath out protons
Body can store some protons
Acidocis is a blood problem
Alkalosis has a high pH of blood
Can lead to hypocalemia
KNOW WHY THEY BOTH LEAD TO THOSE
If extracellular K levels rise what happens to the resting membrane potential? Increase because majority K is inside the cell if its outside find out why?
If extracellular K levels of blood pH drops what happens?
