destroy endometrium lining contraindicated in women who wants kids, make you infertile

Allows identification of common endometrial masses a/w abnormal uterine bleeding (endometrial polyps, submucosal leiomyomas, intracavitary blood clots)

Abnormal babinski

Pimozide treats Tourette syndrome

pneumovax covid-19 vaccine BCG vaccine?

Certain lung cancers, especially squamous cell carcinoma, can produce parathyroid hormone-related protein (PTHrP), which raises blood calcium. Lung tumors that spread to bones can also cause bone breakdown, releasing stored calcium. Elevated calcium promotes tumor growth by activating pathways that increase cell proliferation, inhibit cell death (apoptosis), and maintain inflammation, all of which create an environment conducive to cancer progression and spread.

Pneumonia Emphysema (some type of COPD) Bronchitis Some type of lung cancer (Bronchogenic carcinoma)

Asbetos = Progressive, diffuse pulmonary fibrosis

Direct toxic effect of fibers on pulm. parenchymal cells Mɸ eat them > mediators (ROS, proteases, cytokines, GF) > interstitial pulm. Inflammation and interstitial fibrosis

Catalyzed by iron molecules Can lead to malignancy

Asbestos body: thin central core covered by hemosiderin distributed in a beaded fashion

Linked with Lung cancer (bronchogenic carcinoma > mesothelioma (pleura))

He has thoracic dysfunction, inhalation dysfunction...natural due to his lung issues

since he may have lung cancers we don't want to do anything extreme... myofascial release? rib raising, lymph drainage?

Target chapman's points at the 2nd ICS

CMP CBC TSH CXR PFT

Prostaglandin (PGE) to maintain PDA to help enrich blood

Squatting (increase preload to heart), Oxygenation (occ morphine), medication to increase systemic resistance (phenylephrine), and prostaglandin E (if PDA dependent)

we want the two systems to connect so blood can mix by re-opening the shunts/encourage Ventricular Septal Defect, Ductus Arteriosus, Atrial Septal Defect Prostaglandin infusion: keeps Ductus Arteriosus (PDA) open Rashkind balloon: makes atrial hole (ASD) Jatene procedure: arterial switch operation within the first two weeks of life

watch and wait for spontaneous closures, antibiotic prophylaxis NOT recommended, surgical and transcatheter device used instead

Surgical repair if needed

Prostaglandin

Associations: EtOH exposure, maternal rubella, Down syndrome, 22q11 DiGeorge syndrome

Eisenmenger Syndrome: uncorrected LV → RV shunt from VSD overtime causes volume overload in the right heart and increased right heart pressure, leading to shunt REVERSAL from L → R to R → L → deoxygenated blood spilling into general circulation → O2 decreases → cyanosis

Prenatal circulation = Umbilical veins bring oxygen from mother to fetus. Umbilical arteries bring deoxygenated blood from baby to mother. Three shunts including Ductus Arteriosus skip over the lungs (directly from pulm. a to aorta), so lungs remain collapse. As a fetus, RA pressure > LA pressure. After birth, left sided pressures are higher. Blood goes from high to low pressure.

anterosuperior displacement of the infundibular septum --> the infundibular septum (part of the intraventricular septum) shifts outward and upward, causing PROVe

PROVe Pulmonary Artery Stenosis: causes the right ventricle to have to work harder to push blood through the pulmonary artery. Right Ventricular Hypertrophy: forms as RV work harder and harder against the stenosis. Overriding Aorta: structural problem as the aorta shifts to the middle area, ending up receiving some blood from the right ventricle as well. Ventricular Septal Defect: baby won’t be cyanic if shunt continues from L → R. However, as RVH occurs, pressure increases in the RV, shunting deoxygenated blood from R → L, leading to cyanosis.

CXR CMP CBC Ferritin Iron

Tet Spells: Baby has a VSD to start with, and normally blood goes from LV to RV. But when there's exacerbation of RV outflow obstruction or increase of pulmonary pressure (ex. Exercises, crying, stress), this can lead to R → L shunting and increases cyanosis as deoxygenated blood enters LV then aorta

Not enough oxygenated blood is reaching the body. This can be due to: - Septal defects that cause deoxygenated blood to mix with oxygenated blood --> blood goes from RV to LV - Pulmonary stenosis makes it hard for RV to push blood into the pulm a. to be oxygenated by the lungs

Tetralogy of Fallot Pulmonary Stenosis VSD ASD Eisenmenger Syndrome

S1 = ventricles contract; SL valves open, AV valves close S2 = atrial contract; AV valves open, SL valves close S3 = dilated cardiomyopathy (rapid filling of excess volume of blood into dilated ventricles; overfilled water balloon) S4 = hypertrophied cardiomyopathy (ventricle is stiff, so atria has to push extra hard to get blood into stiffed ventricles)

preload = volume of blood returning to heart to the right atrium

afterload = resistance

contractility = how hard the heart gotta work

Beta 1 adrenergic receptors = gas pedal for the heart, increases HR and contractility

Beta 2, alpha 1 = vasoconstriction

M2 = acetylcholine binds to M2 leads to slowing of heart rate

heart cant pump properly, less blood is reaching the rest of the body

don't take phenylephrine which is worsening the workload of her heart

Dilated cardiomyopathy can lead to atrial fluttering, because heart muscles are stretched and damaged, lead to abnromal condcution

Amlodipine = non-DHP, only works to dilate the blood vessels and has no effects on heart like verapamil (which lowers AV conduction / decreases contractility of the heart)

Phenylephrine = selective alpha 1 agonist, causes vasoconstriction which worsens HTN

more calcium = more contractility

when calcium levels rise it bind to troponin and increase contraction, which increases stroke volume -- more blood pumped out with each beat

Orthopnea is the sensation of shortness of breath (dyspnea) that occurs when a person is lying flat and improves when sitting or standing up. Associated with HF (When lying down, the redistribution of fluid from the lower extremities into the chest increases the pressure on the lungs, exacerbating the difficulty in breathing.)

pulse oximetry = difficulty delivering blood to body

central cyanosis = related too the low oxygen delivery to the body

Jugular Venous Distension = related to right sided HF, dilated and restrictive cardiomyopathy (right atrium pressure builds up because blood keeps regurgitating back to RA, then it backds up into the veins))

Peripheral edema/crackles = from pulmonary congestion since blood be backing up

atrial fluttering atrial fib arrhythmias ventricular tachycardia

HVLA?

electrolyte levels? EKG?

Metoprolol is a selective beta-1 blocker,,,works specifically on the heart to reduce AV node and SA node conduction

Calcium channel blockers

Other drugs that suppress AV node: A....A...

If SA node fails, seek AV node, if AV node fails, seek bundle of his, but the pacemaker rate will be much slower...

First Degree AV Block: prolonged but even PR interval Second Degree: Mobitz Type I (Wenckebach): PR interval lengthening followed by a QRS drop Long long long drop, you have a Wenkebach Second Degree: Mobitz Type II: consistent PR intervals ⇒ low CO symptoms, may progress to third degree. Tx = pacemaker Third Degree (Complete) Heart Block: atria and ventricles beat independently of each other (equal RR and PP intervals) May be caused by MI, degeneration of the conductive tissue, and Lyme Disease (Borrelia burgdorferi)

Delayed transmission?? Slowing the transmission makes it easy for AV conduction block to occur....

Allows for ventricular filling, slow conduction lets the AV valve remains longer

AV node is slow conduction (to encourage ventricular filling), initiated by L-type Ca channels for depolarization; while Bundle of His is fast conduction, initiated by sodium channels for depolarization.

P wave = atrial depolarization P-R wave = atrial contraction QRS = ventricular depolarization S-T = ventricular contraction T-wave = repolarization Q-T interval = the time from beginning of ventricular depolarization to end of repolarization

EKG Troponin CK-MB CMP CBC Lipid panel

Eliminate any tachycardias/atrial fluttesr/atrial fib because they are more tachycardic

Thoracic has significant tart changes, which make sense....

Restricted thoracic inlet on the left, there's restricted lymph node flow

can treat with Diaphragm release technique (thoracic diaphragm release) to help improve lymph node, help with lymph drainage and venous return to the heart (should work for this patient?)

myofascial/soft tissue techniques

Syncope = sudden fainting due to reduction of blood flow to the brain, may be related to her abnormally slow pulse/reduced blood flow to supply body for a moment?

Palpitations = related to problems with disruptions of heart normal electrical activity, so for her she feels like her heart skipped beats with irregular rhythms...heart pauses between beats, reduced blood flow to needed areas

SOB = reduced BF leads to reduced oxygen content being delivered to the body, leading to SOB

HEENT = everything normal, non-remkarable

ABCDE:

A. Asymmetry (of the moles) B. Border (Regular vs irregular border) C. Color (mult shades. etc) D. Diameter (<5-6 mm) E. Evolving (becoming bigger)

Cardiac biomarkers: Troponin, CK-MB CXR Echo CMP EKG

rupture of atherosclerotic plaque thrombus --> clot forms --> so now the clot is partially blocking the blood vessels

Low PO2 and HTN from reduced blood vessels and narrowed blood vessels

Yes it's bad - interferes with COX1 and COX2 stomach function

patients' lipid panel should be measured every 3 months to 1 yr if patients have statin

Percutaneous Coronary Intervention (PCI): performed for 1-2 epicardial coronary a. disease

Coronary Artery Bypass Graft (CABG): perform for 2-3 epicardial coronary a. disease, with objective evidence of myocardial ischemia

Followed by aspirin + clopidogrel

can give BB blocker or CCB with nitroglycerin

(MONABASH = Morphine, Oxygen, Nitroglycerin, Antiplatelets, Beta-blocker, ACE-Inhibitors, Statin, Heparin)

EKG shows elevated ST wave and depressed T wave:

General summary: In AMI, there is transmural injury - infarction damages the entire thickness of the heart across all layers, this is worse than subendocardial injury where only the subendocardium (inner layers of the heart) is damaged

EKG will show inverted T wave ST elevation for STEMI and ST depression for NSTEMI, prolonged Q wave

Normally, ventricles repolarize from epicardium to endocardium. During ischemia or MI, AP duration is reduced, and ventricles repolarizes from endocardium to epicardium instead. This reversed repolarization leads to an inverted T-wave on ECG (negative deflection).

Angina does not change the cardiac biomarkers

Acute MI do --> elevated troponin that peaks and dies faster than CK-MB that takes longer

Troponin I = sensitive and specific, rise in ~4hr and peak in 24hr, lasts 7-10 days

CK-MB: less sensitive and specific, rise in 4-8hr and lasts 48-72 hr (2-3 days), good for looking for reinfarction

Unstable angina, atherosclerotic plaque has ruptured forming a thrombi that partially blocked blood flow

His angina has worsened to an extent where taking nitroglycerin isn't relieving the symptoms

He may be experiencing a side effect of nitroglycerin overdose, ends up having reflex tachycardia and feeling worse

Chapman's reflexes at the bilateral second intercostal spaces - relates to viscerosomatic dysfunction on BETH - Bronchus, Thoracic, Heart, Esophagus

Chapman's reflexes? Counterstrain?

Hypertension due to narrowed blood vessels from atherosclerosis

Low PO2 due to narrowed blood vessels restricting blood flow

Stomach ulcer Prevacid is indicated for the treatment of patients with H. pylori infection and duodenal ulcer disease (active or one year history of a duodenal ulcer) to eradicate H. pylori

HE SMOKES! what does "he thinks he eats good" means...

Unstable angina (probably no longer stable) Myocardial Infarction Pulmonary Embolism, Coronary Embolism, etc (more unlikely because they tend to cause shortness of breath which the patient doesn't have) GERD

CT-Angiography and MR Angiography (most commonly used) (Digital Subtraction angiography is gold standard, but much less used) CMP (patient's hyperlipidemia status) Serum myoglobin D-Dimer CBC (inflammations with tissue necrosis, endothelial cells damage, related to atherosclerosis) HbA1c

Peripheral Arterial Disease (obstruction or deterioration of arteries esp in the lower extremity due to atherosclerosis, most likely) Acute Limb Ischemia (but patient still has pulse in the leg) Atherosclerosis Drug Contraindication with consumption of grapefruit juice (conflicts with statins) Rhabdomyolysis Aortic Dissection of lower limbs? DVT (but patient has a negative homan's sign)

Metabolic Acidosis can cause hyperkalemia --> body tries to get rid of more H+ and in exchange more potassium comes back in

Can treat with diuretics that get rid of potassium (thiazides, loops)

Dependent on ASCVD score, but he should remain a candidate --> has risk of CVD, has atherosclerosis

Reduce LDL levels

1. Identify high risk patient --> Clinical atherosclerotic cardiovascular disease (history of heart attack, stroke, etc.) Diabetes (age 40-75 years) An LDL-C level of 190 mg/dL or higher Individuals aged 40-75 years with an LDL-C of 70-189 mg/dL and a 10-year ASCVD risk of 20% or greater.

2. The guidelines recommend high-intensity statin therapy for the following groups: Adults with clinical ASCVD who are less than 75 years old. Individuals aged 40-75 years with diabetes and an LDL-C level of 70-189 mg/dL. Individuals aged 40-75 years without diabetes but with an LDL-C level of 70-189 mg/dL and a 10-year ASCVD risk of 20% or greater.

Moderate-Intensity Statin Therapy:

Recommended for: Adults aged 40-75 years with diabetes and an LDL-C level of 70-189 mg/dL who are not candidates for high-intensity statin therapy. Individuals aged 40-75 years without diabetes but with an LDL-C level of 70-189 mg/dL and a 10-year ASCVD risk of 5-20%. Lifestyle Modifications:

Emphasis on the importance of lifestyle changes (such as diet, exercise, and smoking cessation) as foundational steps in managing dyslipidemia.

Could have been avoided if patient's does routine checkup for his hyperlipidemia to see if medications are working, should check at least every yr especially since he started statins, but can be more often as every 3 months for his condition

Better counseling: do not take grapefruit juice (CYP Inhibitor) with statins; follow DASH diet, start exercise routine much earlier on to help with weight loss, etc

Dark urine --> rhabdomyolysis/muscle necrosis from tissue ischemia due to lack of blood supply from obstructed blood flow, related to PAD/atherosclerosis, thrombus or emboli that blocks the vessels, grapefruit juice causes elevated statin levels in body that contributes to rhabdomyolysis and myopathy

Right thigh swelling --> obstructed blood flow (from thrombus or atherosclerosis) cause increased pressure in vessels, blood cannot return to heart, leaked out of vessels into surrounding tissues

Homan's negative sign --> not yet DVT, no thrombus yet

Grapefruit juice is a CYP enzyme inhibitor that conflicts with statins' effects --> it inhibits breakdown of statin and elevated statins can lead to myopathy and rhabdomyolosis, both observed in this patient

Secondary causes: Used to smoke a lot Eat fast food here and there Don't drink alcohol "anymore" Doesn't exercise until now (but stands a lot since he works in railroad)

Primary causes: Fam history Mother died from heart attack, may had cardiovascular issues related to hyperlipidemia/HTN, Father has hyperlipidemia, older brother got stroke

Statin (stops the HMG CoA reductase limiting step in cholesterol synthesis) --> helps with patient's hyperlipidemia Lisinopril (-pril drugs) = ACE Inhibitors for his HTN, decrease arterial and venous pressure (by blocking conversion of ANG I into ANG II that pushes for vasoconstriction), decrease aldosterone

Biaxin aka Clarithromycin is an antibiotic for potential upper respiratory infection for his coughs

Bile salts help to emulsify or break down lipids, facilitate lipid solubilization and reabsorption and help it enter enterohepatic circulation

Made from cholesterol

Cholesterol, TG (aka lipids) taken in, brought from intestine to liver by chylomicrons. VLDL brings the lipids to various tissues/adipocytes which are broken down into free fatty acids --> as VLDL gets broken down it becomes VLDL to IDL to LDL (which by then is filled with cholesterol to be delivered to the body), and these all function to bring lipids to the body; HDL bring the lipids from tissues back to liver

Metabolic acidosis: decreased pH, decreased HCO3-, decreased pCO2 (from gaining too much H+ and losing HCO3-; causes: diabetic ketoacidosis, salicylate poisoning); body compensates by hyperventilation (most likely for this patient...may have DM...He is also hyperventilating)

Metabolic Alkalosis: HCO3- stays in body and not released, increase pH; hypoventilation to preserve PCO2 (caused by vomiting or hyperaldosteronism, patient is nauseous but not vomiting), volume contraction alkalosis

Respiratory Acidosis --> decreased pH, increased PCO2- and HCO3-, retention of CO2

Respiratory Alkalosis --> hyperventilation, loss of CO2

Vaping cessation, importance of not smoking at all, precautions when traveling (get all the vaccines needed, for example)

Gram-positive, lancet-shaped, strep-pneumo

Tuberculosis (Pulmonary Infection (but she doesn't have any mucus...but she does have significant weight loss) Pneumonia?

Bacterial Infection (from cuts on arm?) Pulmonary fibrosis (only because patient vapes, chance is lower) COPD Pulmonary embolism (shortness of breath)

Tuberculosis test (TB test) CBC Chest X-ray CMP (ARB, bun/creatinine) Bacterial test Sputum culture test

Ventilation-Perfusion Scanning (?) to see if there's any abnormal perfusion...? more for pulmonary embolism

TORCH =

T: Toxoplasmosis O: Other infections, such as syphilis, varicella-zoster, parvovirus B19, and human immunodeficiency virus (HIV) R: Rubella, also known as German measles C: Cytomegalovirus (CMV) H: Herpes simplex virus (HSV)

Differ in prescribed medication?

Mediastinal shift: mediastinum (contains heart and trachea, etc) shifts away from the normal position at middle of the chest, indicating imbalance in lung pressure -- changes in lung volume, pneumothorax, pleural effusion, lung collapse, etc

Cavitary lesion = a hole in the lungs caused by necrosis of lung tissues that leave behind a cavity, may be due to inflammation after infection like tuberculosis

Hyperdense lobar consolidation = alveolar airspaces filled with fluid, cells or tissues, have higher density in upper lobe of lung, can be caused from some sort of lung hemorrhage

Diffuse Reticular Opacities = indicate lung disease such as interstitial lung disease, indicates scarring of pulmonary interstitiam

Meniscus-shaped density at costophrenic angle = pleural effusion, buildup of fluid around that space, costophrenic angle no longer blunt

Flattened hemidiaphragm = lung is hyperinflated so it pushes down on the diaphragm, happens during emphysema when patient struggles to breathe out, so there's a lot more volume left in lungs

Increased chance of this being a bacterial infection

If patient is 70 y/o...

lung function would have deteriorated, lungs would've lost elasticity; pneumonia, pulmonary fibrosis, COPD, lung cancers risks increase

He went to Brazil which he has a chance of getting Tuberculosis from Mycobacterium, arboviruses such as dengue, and Zika; malaria)

Should not be Dengue because it usually comes with rash and muscle joint pain

Not zika or malaria, no really mention of mosquito sting

Cough = infection, pneumonia, vaping (smoking) that may have already irritated or damaged the airways

Fever = tuberculosis, pneumonia infection, he has cuts on his hand that he got from his job, went to Brazil for vacation

Lung crackles = Fluid in lungs, Fibrosis, COPD, damage from vaping

Person can take ACE-Inhibitors, which treat LVH, aside from lifestyle modifications.

LVH = left ventricles thickened from workload, having to fight against high resistance. ACE-Inhibitors work by inhibiting ANG II formation. This blocks vasoconstriction and aldosterone from acting, promoting vasodilation and reduicing fluid retention.

CMP CBC HbA1c (hemoglobin A1c) EKG (in case) (CT scan?? MRI??? Maybe not that urgent) Urinalysis

Coronary artery calcium score? (need to research on this)

Normal blood pressure is <120 mmhg/<80 mmHg.

Primary = can be idiopathic and polygenic, results of interactions between genetics and environmental factors that are modifyable an unmodifiable. Like family history and eating habits

Secondary = due to associated medical conditions that cause HTN (renal artery stenosis, athersclerosis, etc)

Diet habit, fast food, drinking alcohol, high stress life, multiple coffee intake, history of DM, father's stroke

High work stress, tension headache, alcohol intake, oxycodone side effects

1. Generalized fatigue
2. Chvostek and Troussaeu's sign = hypocalcemia
3. Muscle weakness

TENOFIVIR CAN CAUSE FANCONI SYNDROME = THE INABILITY TO PROXIMAL TUBULE TO REABSORB STUFFS (can explain hypocalcemia)

Can all be related to his HIV, and HIV medications. HIV medications, based on google, can also cause acidosis (reduced H+ secretion, as Na is not being reabsorbed). HIV medications have commonly known to damage the kidneys. Lack of reabsorption may explain his polyuria, his electrolyte imbalances can explain his weakness/fatigue.

the drugs he's taking may impact his thick ascending limb of renal, inhibiting NKCC affects the ability to maintain that lumen positive potential...calcium can't get reababsorbed

Fanconi?

Can be related to her hypernatremia

Aside from CBC, CMP, Na/K/Ca/Mg etc, maybe aldosterone levels as well? and ADH? See if the sodium resorption or water reabsorption hormones are working properly or if the hematoma has damaged these hormones?

She has polyuria and excess urine. Her urine won't be concentrated, she may be peeing out more Na+ or K+, or H+ than she should.

Clonus of lower extremities can indicate some sort of damage to the upper motor neurons? Patient displays hyperreflexia

Upper motor neurons damage = hyperreflexia Lower motor neurons damage = muscle weakness, no response

Normal urine output is 800-2000 mL a day, so she is urinating way too much out.

Risk dehydration, but has input of 125 cc/hr