Final Exam: NR507/ NR 507 (Latest 2024/ 2025 Update) Advanced Pathophysiology Review| Questions and Verified Answers| 100% Correct |Grade A – Chamberlain
Final Exam: NR507/ NR 507 (Latest 2024/
2025 Update) Advanced Pathophysiology
Review| Questions and Verified Answers|
100% Correct |Grade A – Chamberlain
Q: renal calculi
Answer:
Formed by the accumulation of crystalline substances in the urinary tract. A supersaturation of
urine with a stone formation of substances.
Q: Renal calculi nucleation
Answer:
Crystals act as nucleation sites, where further crystal deposition can occur.
Q: Renal calculi crystal retention
Answer:
Urinary stasis or an adequate urine flow allows crystals to remain in the urinary tract
Q: Renal calculi-stone growth and composition
Answer:
Overtime, crystals accumulate and grow into stones
Q: Size kidney stone that can easily be passed on its own
Answer:
< 0.5 cm
Q: Stones likely to cause obstruction
Answer:
1 cm
Q: Type of stone that commonly results from a UTI
Answer:
Struvite stone
Q: Gold standard for diagnosing renal stone
Answer:
CT scan
Q: Most common type of renal calculi
Answer:
Calcium stone
Q: How calcium oxalate stones are formed
Answer:
Urine contains calcium and oxalate. When combined, forms of stone. Citrate and magnesium
will prevent this but people with decreased water intake and increased particle and solute intake,
or decrease magnesium and citrate intake, can get stones.
Q: Dietary recommendations for people with calcium stones
Answer:
Don’t restrict calcium in diet. Encourage balanced diet. Increase hydration.
Q: Treatment for calcium stones
Answer:
Thiazide diuretic to excrete urinary calcium
Q: Why are imaging studies important with renal calculi?
Answer:
They are crucial for assessing the presence, size, location, and compositions of stones. Not all
stones are radiodense and can be seen on x-ray.
Q: Radiodensity of calcium stones
Answer:
Radiodense- seen on X-ray
Q: Radiodensity of uric acid stones
Answer:
Radioluscent- can’t be seen on X-ray
Q: Struvite stones
Answer:
Staghorn stones
Secondary to UTIs, commonly caused by Proteus, Klebsiella, Serratia, Enterobacter
Q: Elements responsible for forming struvite stones
Answer:
Ammonia, magnesium, phosphorus
Q: Pathophysiology of struvite stones
Answer:
Bacteria contribute to stone formation with enzyme urease. Urea and urease change ammonia to
CO2, and makes urine alkaline which favor stone production. Stones of struct renal calyx.
Q: Shape of struvite stones
Answer:
Jagged, irregular, horn-like
Q: Uric acid stones
Answer:
Found in patients with gout and increased uric acid levels
Q: People at high-risk for uric acid stones
Answer:
Those with gout: leukemia, Myelopro- liferic disorder, chemo pts
Q: What does uric acid do to urine acidity
Answer:
Increases urine acidity, which de- creases ph
Q: Treatment for uric acid stones
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Pre-renal causes of AKI Caused by renal hypo perfusion. Due to hypotension, reduced cardiac output, or reduced blood volume.
Intrarenal causes of AKI caused by ATN, acute glomerulonephritis, and other glomerularopathies
Post renal causes of AKI Caused by urinary tract, obstructions, such as BPH, calculi, inflammation, urinary tract tumors.
Reversibility of acute renal failure reversible – if cause treated early enough
Determining prognosis of ARF kidneys respond to diuretic with good UO. This indicates that the kidneys are functioning well.
Acute Pyelonephritis Starts in lower UT, and ascends to kidneys-bacterial colonization (e. coli most common)-adherence and invasion (biofilms created -inflammation and immune response (causes the fever and flank pain associated with disease)-renal injury and complications (sepsis and ARF)
Acute pyelonephritis symptoms Flank painFever Abdominal tenderness * The presence of systemic signs, such as high fever, chills, and tachycardia may suggest severe infection.
Acute pyelonephritis diagnosis UA= +bacteria, +pyuria, (+)WBC CASTSCBC= elevated WBCsImaging= renal US or CT to help identify structural abnormalities and complications, like abscess information or obstruction
Acute pyelonephritis treatment Antibiotics Supportive care: hydration + analgesics (NSAIDS to help manage symptoms and promote recovery)Hospitalization: severe cases, pregnant women, those with underlying comorbidities, or those that cannot tolerate PO intake may require IV antibiotics and close monitoring.Follow up: crucial to monitor treatment response, complete, full course of antibiotics, and ensure resolution of infection through follow up visits and repeat urine cultures.
renal calculi Formed by the accumulation of crystalline substances in the urinary tract. A supersaturation of urine with a stone formation of substances.
Renal calculi nucleation Crystals act as nucleation sites, where further crystal deposition can occur.
Renal calculi crystal retention Urinary stasis or an adequate urine flow allows crystals to remain in the urinary tract
Renal calculi-stone growth and composition Overtime, crystals accumulate and grow into stones
Size kidney stone that can easily be passed on its own < 0.5 cm Stones likely to cause obstruction > 1 cm
Type of stone that commonly results from a UTI Struvite stone
Gold standard for diagnosing renal stone CT scan
Most common type of renal calculi Calcium stone
How calcium oxalate stones are formed Urine contains calcium and oxalate. When combined, forms of stone. Citrate and magnesium will prevent this but people with decreased water intake and increased particle and solute intake, or decrease magnesium and citrate intake, can get stones.
Dietary recommendations for people with calcium stones Don’t restrict calcium in diet. Encourage balanced diet. Increase hydration.
Treatment for calcium stones Thiazide diuretic to excrete urinary calcium
Why are imaging studies important with renal calculi? They are crucial for assessing the presence, size, location, and compositions of stones. Not all stones are radiodense and can be seen on x-ray.
Radiodensity of calcium stones Radiodense- seen on X-ray
Radiodensity of uric acid stones Radioluscent- can’t be seen on X-ray
Struvite stones Staghorn stonesSecondary to UTIs, commonly caused by Proteus, Klebsiella, Serratia, Enterobacter
Elements responsible for forming struvite stones Ammonia, magnesium, phosphorus
Pathophysiology of struvite stones Bacteria contribute to stone formation with enzyme urease. Urea and urease change ammonia to CO2, and makes urine alkaline which favor stone production. Stones of struct renal calyx.
Shape of struvite stones Jagged, irregular, horn-like
Uric acid stones Found in patients with gout and increased uric acid levels
People at high-risk for uric acid stones Those with gout: leukemia, Myeloproliferic disorder, chemo pts
What does uric acid do to urine acidity Increases urine acidity, which decreases ph
Treatment for uric acid stones Increase hydration, increase alkalinity of urine by giving potassium bicarbonate, allopurinol
Clinical symptoms of renal stones Flank or CVA pain (renal colic) Hematuria NauseaVomiting
UA for renal stone Positive for hematuriapH to determine the type of stoneCrystals, infection
US for Renal stone Done for those that cannot do CT scan like for pregnant women. Not the best test though, because they cannot isolate the stone.
Labs for renal calculi Evaluate renal function (GFR)Identify any metabolic abnormalities
Conservative treatment for renal calculi For stones that are less than 5 mm, that are asymptomatic, or causing only mild symptomsControl pain, hydration, observe for spontaneous passage of the stone
Medical management of renal calculi Thiazide diuretics for calcium stonesAllopurinol for uric acid stones Stone removal for stones larger than 5 mm or stones, causing severe symptoms – lithotripsy
Goals of treatment for renal calculi Manage acute painPromote passage of the stone Reduce the size of the stone already formed Prevent new stone formation
chronic kidney disease The progressive loss of renal function associated with systemic diseases, such as hypertension, diabetes, mellitus (most significant risk factor), systemic, lupus, erythematosus, or intrinsic kidney disease
Stage 1 CKD GFR 90-120There is damage to kidney with normal or increased GFR
Stage 2 CKD GFR 60-89There is kidney damage with mild decrease in GFR
Stage 3 CKD GFR 30-59There is moderate decrease in GFR* This is a significant phase! GFR below 60- still a chance to improve function and avoid dialysis.
Stage 4 CKD GFR 15-29There is severe reduction in GFR .Once this stage is reached, progression to the next stage is inevitable, as well as dialysis or kidney transplant being necessary .
Stage 5 CKD GFR <15Needs dialysis or kidney transplant Dialysis and so determining who is the candidate for dialysis Based on symptoms, kidney function, overall health status, individual circumstances Six reasons for dialysis 1. Metabolic acidosis. (Low pH)2. Hyperkalemia, with EKG changes – peaked T waves. 3. Drug toxicity (salicylates, lithium, isopropanolol, methanol, Etheline glycol).4. Fluid overload (not responding to diuretics)/ HTN/ pulmonary edema5. Uremic symptoms – due to nitrogenous waste in bloodstream.6. Progressive loss of kidney function. Number one cause of ESRD DM + HTN combined Why anemia occurs in ESRD Reduce production of erythropoietin, which is responsible for triggering the production of RBCs, rather than the lack of iron or a reduction in the RBCs Symptoms of CKD •Hypocalcemia and hyperphosphatemia•Anemia • hyperkalemia With abnormal EKG findings and elevated T waves• Excess hydrogen ions, causing metabolic acidosis• Uremia, which can cause pericarditis, encephalitis, bleeding, and increased risk of infections (the second most common cause of death for end stage renal disease patients)• Fluid volume overload-diuretics can be used to stimulate renal function for patients in stage 1 to 3. If diuretic therapy fails, or if in stage four or five and dialysis is indicated. What causes fluid volume overload in chronic kidney disease? Due to inability of the kidney to filter fluid through the glomerulus due to a reduced GFR CKD diet Low potassium low sodium/waterphosphate bindersAdequate protein Fluids and CKD Fluid restriction of 500 cc to 1 L per day or the amount that does not cause overload Ace inhibitors with CKD Lisinopril, enalapril, captopril are used to provide renal protection in stages 1-3 Medication Avoidance with CKD. Avoid nephrotoxic medications like NSAIDs and aminoglycosides (gentamicin, Neomycin, tobramycin) Bacteria associated with GERD H. Pylori Causes of GERD Incompetent lower esophageal sphincter, hiatal hernia, Gastroparesis (esophageal motility disorder), obesity, acidic acid contents Esophageal Motility Disorders Impaired esophageal peristalsis and reduce esophageal clearance can lead to pooling of gastric acid in the esophagus. hiatal hernia Diaphragmatic weakness (muscle of respiration) Sliding hiatal hernia- most common type. Diaphragmatic hernia that protrudes or herniates through the upper part of the stomach through the diaphragm, and into the thorax, due to dilation of the Gastroesophageal junction How does hiatal hernia relate to GERD? Contributes to GERD by disrupting the normal barrier between the esophagus on the stomach How do acidic acid contents of the stomach relate to GERD? Acidic contents reflux back into the esophagus and directly damage, the mucosal lining of the esophagus which triggers a huge inflammatory process. This causes the characteristic symptoms of GERD. Subjective symptoms of GERD Heartburn (burning sensation in chest)Regurgitation (acidic taste in the mouth)Dysphagia Chest pain -(may mimic cardiac chest pain, so it is necessary to rule out a cardio clause). Objective symptoms of GERD Physical exam is usually normal in uncomplicated cases, although there may be signs of esophagitis or other complications in severe cases. Diagnostics tests for GERD For severe or persistent cases: Upper G.I. endoscopy, esophageal pH monitoring, and esophageal manometry Diagnosing GERD -look at clinical symptoms-before we do diagnostic tests, check response to empiric therapy such as a proton pump inhibitor (PPI) -diagnostics tests Treatment for GERD -Lifestyle modification: avoid trigger foods (chocolate, caffeine, alcohol, spicy food, and acidic foods). -Weight loss (esp for BMI > 25)-Elevate head of bed-Avoid food for 2 to 3 hours before bed-portion control-meds: PPI, H2R, PKA-Surgery
Meds for GERD Meds: PPI (protonix), H2 receptor antagonists (famotadine), prokinetic agents to improve esoph motility (reglan)
Warning signs of GERD Common over age 50DysphasiaOdynophagia (pain with swallowing)NauseaVomiting Weight loss MelenaEarly satiety
Can indicate bleeding when combined with GERD Iron deficiency anemia
Sliding hiatal hernia Where the junction of the esophagus slides up past the GE junction. The proximal portion of the stomach moves into the thoracic cavity through the esophageal hiatus, and opening in the diaphragm for the esophagus and the vagus nerves
What exacerbates sliding hiatal hernias Coughing, bending, Valsalva maneuver, wearing tight clothing, ascites, obesity, or pregnancy
Contributing factors to hiatal hernia Increased age, obesity, pregnancy, increased, intra-abdominal, pressure, structural abnormalities of the diaphragm
Relation of sliding hiatal hernia to GERD Diminishes the resting pressure of the LES
Symptoms associated with hiatal hernia Patients who present with hernia are often asymptomatic, if symptoms, to develop their usually later in life, and associated with GERD:Heartburn Regurgitation Dysphasia Epigastric pain
Complication of hernia Strangulation is a complication can lead to ischemia
Symptoms of a strangulated hernia Acute, severe epigastric, or chest painNausea Vomiting G.I. bleeding
diagnosis of hernia Symptom assessmentUpper GI barium swallow or EGD
Hiatal Hernia Treatment -Lifestyle modificationEating small, frequent meals and avoiding the recumbent position after eating Avoid tight clothes and abdominal supports.Weight loss -Meds: PPI for reflux, antacid, prokinetic agents-surgery
duodenal ulcer Occurs in the lining of the upper most part of the small intestine just after the stomachMost commonly due to H. pylori infection, which resulted in inflammation and ulceration of the gastric mucosa
patho of duodenal ulcers Hypersecretion of stomach acid by parientas cells and pepsin- occurs primarily due to NSAID use and smokingImpaired mucosal defense mechanisms Disruption of balance between aggressive and defensive factors
risk factors H. Pylori infectionRegular NSAID useSmoking hxHx ulcer or GIB
Symptoms of Duodenal ulcer -Chronic intermittent pain in the epigastric area-Pain begins 30 minutes to 2 hours after eating when the stomach is empty It is not unusual for pain to occur in the middle of the night and disappear by morning.-Stomach pain that is relieved after a meal/antacids-GIB
Physical exam with duodenal ulcer usually completely normal
Diagnosis for duodenal Ulcer Upper G.I. endoscopyH. Pylori Testing Imaging studies hx and symptom assessment Is there an increased risk of cancer with duodenal ulcer? No increased risk Duodenal ulcer treatment Medications: PPIs, H2RB, abx for h. Pylori, antacids and cytoprotective agents (carafate). Colloid bismuth. Anticholinergics to delay gastric emptying/secretion. Lifestyle modifications: no smoking, reduce alcohol, manage stress, reduce/avoid NSAIDs. Diet: high fiberSurgery for complications Follow up/monitoring Peptic Ulcer Disease (PUD) A break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum. Severe inflammation occurs and can penetrate the sub mucosa . This is least likely to occur in the large intestine. Risk factors for PUD NSAIDsH. Pylori infectionASA useGenetic predisposition Alcohol use Smoking Pancreatitis COPD Acute stress Protective mechanisms against risk factors for PUD Mucus and bicarbonate secretionProstaglandins Mucosal blood flow Epithelial cell renewal symptoms of peptic ulcer disease Abdominal pain or discomfort (epi gastric), heartburn, indigestion, unintentional weight loss, nausea and vomiting Physical exam: typically unremarkable if uncomplicated, but if it’s a severe case, they may have some abdominal tenderness and possibly some signs of G.I. bleeding (blood in stool, vomiting blood). Diagnostics for PUD EndoscopyH. Pylori testingImaging studies Treatment of Peptic Ulcer Disease (PUD) Medications:PPI, Abx, H2RB, cytoprotective agentsLifestyle modification:Avoid NSAIDsSmoking CessationDietary changes Follow up and maintenance therapy Major Depressive Disorder (MDD) Psychological disorder with a neurotransmitter imbalance involving serotonin, norepinephrine, and dopamine. Patho of MDD Neuro endocrine dysregulation caused by abnormalities in the hypothalamic -pituitary-adrenal access, which causes elevated cortisol levels (primary stress hormone). Causes detrimental effect on brain structure which regulates mood and causes depressive mood.Chronic inflammation/inflammatory processes theoryNeuroplasticity and structural changes First line treatment for major depression SSRIsCitalopram (Celexa)Escitalopram (Lexapro)Fluoxetine (Prozac)Fluvoxamine (Luvox)Paroxetine (Paxil) Sertraline (Zoloft) How to select antidepressant for MDD Consider assessment of person’s symptoms’AgeSide effectsSafetyCost social anxiety disorder Fear and avoidance of social disorder Example: the person may feel very uncomfortable, having a conversation or interacting with others, and feel very conscious of being scrutinized and humiliated or rejected by othersMay skip events completely Interferes with a patient’s normal routine and relationships with others Causes distress and anxiety in specific social situations like making small talk with others, meeting, new people, performing in front of others, – performance anxiety social anxiety disorder Ego-dystonic condition – patient knows their anxiety is unwarranted, which causes more anxiety due to fear that others can perceive anxiety felt by themIf severe enough derealization occurs in a person, feel spaced out and unable to recognize surroundings Not the same as agoraphobia, which is the fear of being trapped or not being able to escape in something embarrassing occurs panic disorder Involves a very stressful situation where individual develops an intense fear something bad will happen.Eminent threat, or danger is perceived Feelings are intense and accompanied by physiological symptoms like palpitations, dizziness, shortness of breath. Symptoms can peak in the first 10 to 20 minutes booking last hours. Person might feel like they are having a heart attack or other life-threatening illnesses. Attacks are unpredictable. Treatment for panic attacks Cognitive behavioral therapyAntidepressants (SSRIs)Benzodiazepines Anti-seizure medication’s for severe panic attacks Generalized Anxiety Disorder (GAD) Excessive, persistent, and unreasonable anxiety about every day situations involving money, work, family, and relationships.Even the thought of getting through the day can provoke anxiety Symptoms of Generalized Anxiety Disorder (GAD) WorryAnxiety Edginess Restlessness Difficulty concentrating Difficulty sleeping/chronic fatigue Irritability Digestive problems-over/under eatingMuscle aches due to tension Treatment for anxiety disorders Psychotherapy/cognitive behavioral therapyMedications: BenzodiazepinesAntidepressants (SSRIs)Beta blockers (for SAD) Schizophrenia Scattered fragmented pattern of thinking. Cause is mostly unknown, but thought that it is related to increased dopamine levels. positive symptoms of schizophrenia Psychotic symptoms:Hallucinations, delusions, formal thought disorder, bizarre behavior Negative symptoms of schizophrenia The removal or reduction of normal processes:Flattened affect, alogia, anhedonia, Attention deficits, and apathy. cognitive symptoms of schizophrenia Issues with being able to remember things:Memory Ability to learn Understanding The symptoms are subtle, and may only be detected when specific tests are performed. For example, individual may not be able to keep up with several tasks at once. Diagnosing schizophrenia Structural brain abnormalities on neuroimaging: Enlargement of the lateral and third ventricles, and the widening of frontal cortical fissures and sulci Alogia A lack of content in the speech. A negative symptoms of schizophrenia. Avolition A decrease in motivation to complete certain goals Hypothyroidism Most common disorder of the thyroid functionHappens when the thyroid does not produce enough, hormones, resulting in a low metabolic rate, combined with slow respiratory and cardiovascular activities TSH (thyroid stimulating hormone) Released by the anterior pituitary How prevalent is hypothyroidism? Affects between 0.1 and 2% of the US population.More common in the women and the elderly Alzheimer’s disease Decreased short term memory occurs with mild cognitive decline as a result of reduced hippocampus size Accumulation of abnormal amyloid, beta proteins structures in the brain leads to plaque formation in AD Amyloid, beta plaques neurofibrillary tangles of AD Formation of tangles, composed of hyperphosphorylated tau protein, disrupting neuronal function Neuronal dysfunction and loss in Alzheimer’s Widespread neuronal dysfunction and loss in affected brain regions, causing impaired cognitive processes Neurotransmitter imbalance in AD Alterations in acetylcholine, glutamate, and serotonin levels affect memory, cognition, and mood Inflammation and Oxidative Stress in AD Chronic inflammation and increase oxidative stress contribute to neuronal damage Vascular changes in Alzheimer’s Vascular dysfunction and reduced blood flow to the brain impact oxygen and nutrient delivery What stage can you diagnose Alzheimer’s dementia ~Stage four – mild Alzheimer’s Math – very challenging Memory declines Sequential tasks like cooking and driving are too hard Can still recognize family and friends Diagnosis of Alzheimer’s No one test, need to complete assessment and to rule out other medical causes like medication, trauma, vascular issuesMRI to reveal hippocampus atrophy Parkinson’s disease Movement disorder where the dopamine – producing neurons, and substantia nigra of the brain undergo degeneration Onset of Parkinson’s disease Adulthood Loss of dopamine producing neurons with Parkinson’s Selective loss of dopamine producing neurons in the substantia nigra lead to dopamine deficiency Lewy bodies and Parkinson’s Abnormal protein aggregates (primarily alpha-synuclein) that accumulate in neurons contribute to neuronal dysfunction and degenerate Impaired mitochondrial function in Parkinson’s Dysfunction of mitochondria lead to reduced energy production and increased oxidative stress Oxidative stress & free radicals – Parkinson’s Increase production of free radicals and oxidative stress contribute to cellular damage Neuroinflammation in Parkinson’s disease Inflammatory response in the brain is involved in activating microglia and release of pro-inflammatory molecules Alpha-Synuclein spreading in PD Propagation of alpha-synuclein pathology from cell to cell contributes to progressive neurodegeneration bradykinesia Slow movement associated with shuffling gait in PD Motor Symptoms of Parkinson’s disease Bradykinesia with shuffling gaitResting tremor – involuntary, mostly noted in hands. Pin rolling movement. Diminishes with movement.Rigidity Postural disturbance (late feature and can lead to falls) Non-motor symptoms of Parkinson’s disease Cognitive changes (dementia)Mood disorders (depression)Sleep disordersAutonomic dysfunctionSensory symptoms (difficulty smelling)Speech and swallowing difficultiesFatigue Multiple Sclerosis (MS) Demyelinating disease of the CNS that includes the brain and the spinal cord.Demyelination occurs when the immune system in appropriately attacks and destroys the mile in which breaks down communication between neurons, ultimately resulting in sensory, motor, and cognitive problems What type of a hypersensitivity reaction is multiple sclerosis Type 4 hypersensitivityCell-mediated Risk factors for multiple sclerosis SmokingVitamin D deficiency Epstein-Barr virus Symptoms of MS Poor concentration in critical, thinking, depression, anxiety, bowel and bladder symptoms sensation from the skin like pins and needles. Chariot’s triad. Lhermitte’s sign. Charcot’s Triad Neurological triad associated with MS:Dysarthria Nystagmus Intention tremor Lhermitte’s sign An electric shock that runs down the back and radiates to the limbs when bending neck forward. Associated with MS. Immune system dysfunction in MS Abnormal immune system response to targeting myelin in the CNS. Activation of immune cells, particularly T cells, leading to inflammation and demyelination. Inflammation and demyelination in MS Inflammatory response in the CNS results in the destruction of myelin sheath surrounding the nerve fibers Axonal damage and neuron degeneration in MS Loss and degeneration of nerve fibers (axons) as a consequence of repeated episodes of demyelination and inflammation Reactive gliosis in MS Activation and proliferation of glial cells, particularly astrocytes and microglia, in response to CNS injury Remyelination attempts in MS Efforts to repair damaged myelin through remyelination processes occur, although these attempts are often incomplete and not fully successful Possible motor symptoms of MS Weakness, paralysis, spasms, tremors, coordination, and balance, problems, fatigue Possible sensory symptoms of MS Numbness, tingling, altered sensations, MS hug Possible Visual symptoms of MS Optic neuritis, double vision, eye-movement abnormalities Possible cognitive and emotional symptoms of MS Memory problems, attention difficulties, slowed information, processing, emotional changes Possible bowel and bladder dysfunction in MS Urinary frequency, urgency, difficulty in emptying the bladder, constipation, bowel incontinence Possible sexual dysfunction symptoms in MS Reduce libido, erectile dysfunction, decreased vaginal lubrication Possible speech and swallowing difficulties in MS Slurred or swallowed speech, difficulty swallowing Heat intolerance with MS Worsening of symptoms with exposure to heat or hot weather Fatigue with MS Profound fatigue, and lack of energy Febrile seizures cause Neurons are excited by decreased CO2 levels caused by hyperventilation during a febrile stateHR + RR increase to blow off CO2 cluster headache Typically one-sided, often around the eye or temple. Intense, severe pain, often described as sharp or piercing – pain can be referred to the mid face or teeth.Short, typically lasting 15 mins to 3 hours (rarely up to 3 hours) Cluster headache triggers Alcohol, certain foods, strong smells, high altitude Frequency of cluster headaches Often occurs in clusters or cycles, with multiple attacks per day, for weeks to months, followed by periods of remission Associated symptoms with cluster headaches Ipsilateral autonomic symptoms:Redness in tearing of the eye, nasal congestion, drooping eyelidRestlessness Prevalence of cluster headaches More common in men, between 20 and 50 years of ageFamilial tendency Migraine headaches One-sided, and can spread to other areas of the headThrobbing or pulsating pain Can last from 4 to 72 hours Frequency of migraine headaches Can vary widely from occasional episodes to several times a month Associated symptoms of migraine headaches NauseaVomiting Photophobia Phonophobia Aura Prevalence of migraine headaches More common in womenFamilial tendency Classifications of migraines 1- migraine with aura with visual, sensory, or motor symptoms 2- migraine without aura (most common)3- chronic migraine Migraine triggers Stress, hormonal changes, certain foods (alcohol are nitrates), sensory stimuli (like bright lights, strong smells), lack of or too much sleep, missed meal tension headache Most prevalent type of recurrent headacheUsually a mild to moderate bilateral headache with a sensation of a tight band or pressure around the head Can last from 30 minutes up to several days Frequency of tension headaches Can be episodic (less than 15 days per month) or chronic (15 or more days per month) Associated symptoms of tension headaches Mild sensitivity to light and soundNO nausea or vomiting Tension, headache triggers Stress, anxiety, poor posture, muscle tension Tension headache prevalence Equally common in men and womenFamilial tendency Average age of onset is during the second decade of life Bell’s palsy is associated with what cranial nerve Cranial nerve VII Bell’s palsy Associated with cranial nerve VII paralysis and results in facial asymmetry, and in ability to close eye, smile, or frown on the affected side Trigeminal neuralgia affects which cranial nerve? Cranial nerve V trigeminal neuralgia Associated with compression of cranial nerve, five and results in severe and sharp, stabbing pain that can worsen with chewing Bacterial Meningitis symptoms Clinical manifestations of systemic infection: fever, tachycardia, chills Clinical manifestations of meningeal irritation Severe, throbbing, headache, severe photophobia, nuchal, rigidity, positive Kernig, sign, positive Brudzinski sign Kernig sign- poisitive Straightening the knee with the hip and knee in a flex position produces pain in the back and neck regionsIndicative of meningeal irritation Brudzinski sign – positive Passive flexion of the neck produces neck pain and increased rigidityIndicative of meningeal irritation bacterial meningitis treatment Steroids, followed by antibiotics to prevent information that can be caused by antibiotics as they destroy bacteriaPrevention using vaccinations Prophylactic antibiotics to avoid outbreaks Classic triad of meningitis HeadacheFever Nuchal rigidity Infarct in ACA Results in motor: contra lateral paralysis or paresis (greater in foot and thigh) Sensory deficits with basilar artery infarct Contralateral loss of vibratory sense, sense of position with dysmetria, loss of two-point discrimination, impaired rapid alternating movements. Rosacea triggers Exposure to extreme temperaturesStrenuous exercise Severe sunburnStress and anxiety Hot and spicy foods Alcohol ingestion Caffeine Certain medicationsHormonal fluctuations H. PyloriDemodex mitesPresence of cathelicidin Rosacea Familial tendency with several genetic factors involvedInvolves neurovascular, dysregulation, infection, and factors that trigger altered innate and adaptive immune responsesCauses a stinging and burning facial rash – common inflammatory skin disorder, primarily of the face Melanoma Most aggressive skin cancerThe thickness of the lesion impacts the prognosis ABCDEs of melanoma asymmetry, border, color, diameter, evolution Plaque Psoriasis Typical lesion is well-demarcated, thick, silery, erythematous plaque surrounded by normal skin that can appear anywhere on the body Hypoglycemia neurogenic reactions TachycardiaPalpitations Diaphoresis Tremors Pallor Arousal anxiety Growth Hormone (GH) Stimulates, growth, cell production, and regenerationReleased by the anterior pituitary Prolactin (PRL) Stimulates milk, production in lactating womenReleased by the anterior pituitary Thyroid Stimulating Hormone (TSH) Stimulates the thyroid gland to produce thyroid hormonesReleased by the anterior pituitary adenocorticotropic hormone (ACTH) Released by the anterior pituitaryStimulates the adrenal glands to release cortisol, a stress hormone Follicle-stimulating hormone (FSH) Stimulates the production of eggs in females in sperm in malesReleased by the anterior pituitary luteinizing hormone (LH) Triggers ovulation in females and stimulates testosterone production in malesReleased by the anterior pituitary How is the anterior pituitary stimulated to release hormones It receives releasing hormones from the hypothalamus. Hypothyroidism Decrease production of thyroid hormone in the thyroid. The hypothalamus will secrete more thyroid releasing hormone (TRH) to stimulate the anterior pituitary to secrete more thyroid stimulating hormone (TSH) to stimulate the thyroid follicles to secrete more thyroid hormone (T3 & T4). Diagnostic labs in hypothyroidism High TSH levelsLow total, T3, T4, and free T4 symptoms of hypothyroidism Weight gainConstipationHair lossgoiter (d/t increased TSH production)Fatigue Bradycardia Coldness Lethargy Poor memory/concentrationAscitesBrittle hair and nailsDepressionSOBpericardial effusionPleural effusionParesthesia Treatment of hypothyroidism Levothyroxine (Synthroid) Primary hypothyroidism Thyroid is stimulated properly, but is unable to produce enough thyroid hormones for the body to function properly, because the issue is the thyroid gland itselfEx: Hashimoto’s Autoimmune Thyroid Disease secondary hypothyroidism The pituitary is not stimulating the thyroid to produce enough hormones- the gland is not the problem. Ex: pituitary tumor or hypothalamic tumor, or radiation to tumor in brain affect hypothalamus function Hyperthyroidism Excessive production of thyroid, hormones by the thyroid gland. Most common cause of hyper thyroidism Graves’ disease Graves’ disease An autoimmune disorder in which the immune system stimulates the thyroid gland to produce more hormones (T3 & T4). Two of the most distinguishing factors of Graves’ disease ExophthalmosPretibial myxedema 2 categories of opthmalmopathy in Graves’ Functional abnormalities Infiltrative changes Functional abnormalities of opthalmopathy Infiltrative changes of opthalmopathy in Graves’ Hyperthyroidism treatment Goal: control, excessive TH production, secretion, or actionMedication: anti-thyroid drug therapy (methimazole or propylthiouracil)Radioactive iodine therapy: absorbed only by thyroid tissue, causing death of cellsSurgery pretibial myxedema dry, waxy swelling of the front surfaces of the lower legsDoes not get reversed with treatment of hyperthyroidism, but can be treated with topical steroids for skin lesion flareups Goal of radioactive iodine ablation For the treatment of Graves’ disease – to destroy overactive thyroid tissue type one diabetes mellitus Auto immune – genetic and environmental factors that result in the gradual process of autoimmune destructionOnset <10-20 years of ageAssociated with DKA Presenting symptoms of Type 1 diabetes Presenting symptoms: Polyuria, polydipsia, polyphagia Factors associated w/ type 1 diabetes Viral infections, particularly enteroviruses, Coxsackie, virus, other infectious microorganismsH. PyloriExposure to cow’s milk protein Lack of vitamin D Weak genetic associationNot associated with obesity Diagnostic criteria for diabetes mellitus Hemoglobin A1C > 6.5% action of insulin Promotes glucose uptake, mostly in the liver, muscle, and adipose tissue Autonomic neuropathy complications of diabetes Decreased esophageal motilityGastroparesis Delayed gastric emptying secretion of parathyroid hormone Stimulated by hypocalcemiaIncreases calcium levels and decreases phosphate levels Primary hyperparathyroidism causes Parathyroid gland tumorHyper function of the parathyroid cells due to adenoma = hypercalcemia Secondary hyperparathyroidism Arises as a compensatory response to chronic low calcium or vit D levels Increased PTH secretion in response to hypocalcemia Causes of secondary hyperparathyroidism CKD as PTH increases, it could lead to hypercalcemia
Hypercalcemia Goes with hypophosphatemiaDue to increased PTH
symptoms of hypercalcemia Asymptomatic or symptoms related to neuromuscular changes that include paresthesias and muscle cramps, Weakness, decreased deep tendon reflexes
Patients with _ can have () that is most noted in the distal 1/3 of the radius. HypercalcemiaLow bone density Osteoporosis
Issues associated with hypercalcemia Kidney stonesPathological fractures Ventricular hypertrophy Depression Gastric issues (anorexia, nausea, vomiting, heartburn, constipation, abdominal pain, weight loss)
Hypoparathyroidism Low magnesium can cause a decrease in PTH secretionAbnormally low PTH level can be caused by damage or removal of PTH gland during surgery. Can also be associated with genetic syndrome (DiGeorge), autoimmune, or familialLow Ca+ /High phos
Causes of hypomagnesemia (for hypoparathyroidism) •Chronic alcoholism•Malnutrition •Malabsorption •Increased renal clearance of magnesium caused by the use of aminoglycoside antibiotics or certain chemotherapy agents or prolonged magnesium deficient parental nutritional therapy
Signs of hypocalcemia Dry skinLoss of body and scalp hair Hypoplasia of developing teethHorizontal ridges on the nails Cataracs Basal ganglia calcifications Bone deformities Bowing of the long bones
Treatment of hypoparathyroidism IV calciumPO calcium and active vitamin D for maintenance PTH replacement therapy with recumbent human parathyroid hormone to decrease the need for supplemental calcium and vitamin D
Hypercortisolism A condition caused by prolonged exposure to cortisol, mainly due to overproduction of ACTH (adrenocorticotropic hormone) by the pituitary
Causes of hypercortisolism Cushing disease (pituitary tumors)Adrenal tumors
Cushing disease Hypercortisolism caused by a pituitary tumor that excretes excess ACTH (causing excess cortisol)
How do adrenal tumors cause hypercortisolism? Produces cortisol independent of normal regulatory mechanism of the HPA axisSuppression of ACTH – due to high cortisol levels that exert negative feedback on the pituitary gland and hypothalamus which inhibits secretion of ATCH
Symptoms of hypercortisolism Glucose intoleranceWeight gain Muscle wasting
Cause of glucose intolerance in hypercortisolism Excess cortisol causes insulin resistance, and an increase in glyconeogenesis and glycogen storage in the liver
Cushing syndrome characteristics Truncal obesityMoon phase Buffalo hump
Treat hypoglycemia with Simple carbohydrateDextrose Glucose
Hypocortisolism adrenal insufficiencyInsufficient cortisol production Lack of aldosterone Stress response failure
primary hypocortisolism Addison’s diseaseDue to a primary problem in the adrenal gland, that prevents the production and secretion of adrenocortical hormones
Adrenal crisis symptoms HypotensionFeverSyncope Convulsions Hypoglycemia Hyponatremia Severe vomiting and diarrhea
Adrenal crisis triggers InfectionSurgery Trauma Sudden discontinuation of corticosteroid therapy
Onset of adrenal crisis is signified by what? Hypotension
Addisonian crisis Aka adrenal crisisHypotension that progresses to complete vascular collapse and shock with hypocortisolism. Develops with undiagnosed disease, or acute withdrawal of glucocorticoid therapy, or the occurrence of infection, or other comorbid stressful event
Labs associated with primary hypocortisolism -Low serum and urine cortisol levels-ACTH levels increased
Treatment for primary hypocortisolism /adrenal insufficiency Corticosteroid replacement therapy -Lifetime replacement (Hydrocortisone, prednisone, methylprednisolone)-Increase dosing during infection, surgery, trauma, or any acute stressors… then reduced after
Most common cause ok AKI Pre renal causes
CKD stage based on GFR and albuminuria
What part of the melanomas skin lesion impacts the prognosis? The thickness
Treatment of hyperparathyroidism Avoid dehydration and decrease calcium intake in the asymptomatic patient.Severe primary- surgeryCalcimimetics (cinacalcet) and biphosphonates if surgery fails.Secondary- watch renal function
Tetany goes with Hypocalcemia
Chovstek’s sign a clinical finding associated with hypocalcemia, or low levels of calcium in the blood. This clinical sign refers to a twitch of the facial muscles that occurs when gently tapping an individual’s cheek, in front of the ear.