What is Pathology - Respiratory Acidosis
Pathophysiology
• The body's pH should range from 7.3 to 7.45. The pH is low, CO2 is high, and HCO3 is either within the normal range or increasing to make up for it, indicating respiratory acidosis according to the ABG analysis.
• When the pH fluctuates, the body activates buffering mechanisms. Cellular reserves are the first to respond. In respiratory acidosis, K+ is shifted out of the cells as a result of H+ being taken into the cells.
• The second buffering mechanism to engage is the lungs. Low pH causes rapid and deep respirations, which produce CO2.
• The kidneys are the final buffering mechanism, and it can take them up to two days to start modifying pH. The kidneys produce H+ when there is respiratory acidosis.
• The use of drugs that impair lung function, hypoventilation, sleep apnea, and COPD are some of the causes.

Assessment and diagnostic findings include CXR, drug testing, polycythemia screening on the CBC, and ABG analysis.

Complications include changes in mental state, cerebral edema, and papilledema as a result of chronic hypoxemia, which can also cause polycythemia, pulmonary hypertension, and cor pulmonale. Death might happen.

Medical Attention and Surgical Procedure
• Bronchodilators, mechanical ventilation assistance, naloxone or flumazenil for benzodiazepine and opioid overdoses, and theophylline.
• Surgical procedures for treating weight and sleep apnea.
• Teach the client how to maintain a healthy weight, abstain from smoking, and use oxygen as advised.
• Inform the customer about available sleep study options.
• Keep an eye on your ABGs, breathing, and CBC levels for polycythemia.
• Determine the brain edoema score on the Glasgow Coma Scale and the presence of papilledema.

What is Pathology - Metabolic Alkalosis
Pathophysiology
• The body's pH should range from 7.3 to 7.45. The pH is high, the CO2 is within the normal range or rising to make up for it, and the ABG identifies metabolic alkalosis.
• When the pH fluctuates, the body activates buffering mechanisms. Cellular reserves are the first to respond. In metabolic alkalosis, potassium ions (K+) are shifted into the cells as a result of H+ being discharged from the cells.
• The second buffering mechanism to engage is the lungs. High pH causes CO2 to be retained by shallow, slow respirations.
• The kidneys are the final buffering mechanism to activate, and it could take them up to two days to start influencing pH. In metabolic alkalosis, H+ is stored in the kidneys.
• The use of loop diuretics, antacids, licorice, glucocorticoids, and mineralocorticoids are among the causes, as are prolonged vomiting, gastrointestinal suction, diarrhea, and these conditions.

Evaluation and Diagnostic Results
• Hypocalcemia and hypokalemia; urine chloride less than 20 mEq/L; ABG measurement.
• Errors on the ECG (ECG).

Symptoms of complications include tetany, seizures, altered mental status, hypoventilation and hypoxemia, and fatal arrhythmias (K+).

Medical Attention and Surgical Procedure
• Corticosteroids, nonsteroidal fluid replacement, IV hydrochloric acid formulations, potassium-sparing diuretics, ACE inhibitors, K+ and Ca supplements, and fluid replacement.
• Inform patients about metabolic alkalosis, particularly when they experience prolonged vomiting, and urge them to see a doctor if their mental state changes or if they tremble.
• Keep track of ABGs and other lab results. Check the ECG for arrhythmias linked to low K+ levels and both Chvostek and Trousseau's signs to identify low calcium levels.

What is Pathology - Metabolic Acidosis
Pathophysiology

• The body's pH should range from 7.3 to 7.45. ABG measurement identifies metabolic acidosis due to low pH, normal or compensatory CO2 levels, and low HCO3 levels.
• When the pH fluctuates, the body activates buffering mechanisms. Cellular reserves are the first to respond. In metabolic acidosis, K+ is shifted into the extracellular space as a result of H+ being taken into the cells.
• The second buffering mechanism to engage is the lungs. Low pH causes rapid and deep respirations, which produce CO2.
• The kidneys are the last buffering mechanism to activate; it could take them up to two days to start influencing pH. The kidneys produce H+ when there is metabolic acidosis.
• Diarrhea (loss below the waist), CRF, lactic acidosis, salicylate poisoning, methanol and alcohol poisoning, paraldehyde poisoning, and diabetic ketoacidosis are some of the possible causes.

Evaluation and Diagnostic Results
• Low pH and HCO3 levels. Further testing is guided by the anion gap value, which can be large, low, or normal.
• Kussmaul's respirations, a shift in mental state, blood chemistry analysis for azotemia, electrolytes, and high fasting glucose levels, serum osmolality, and ECG changes.
Complications
• A persistent acid-base imbalance can cause mortality.

Medical Attention and Surgical Procedure
• IV sodium bicarbonate infusion; pH balance adjustment.
• Inform the customer about environmental toxins.
• Explain to the customer the warning signs and symptoms of diabetes mellitus and the significance of keeping blood sugar levels normal.
• Keep an eye on your test results, mental status, acetone breath, and ECG.

What is Pathology- Graft-Versus-Host Disease
Pathophysiology
• Following a solid organ, bone marrow, or stem cell donation, GVHD may develop. The host cells are regarded as alien by the graft cells.
• Chemotherapy and radiation treatment were used to prepare the host tissue for transplant, which is where Phase 1 of GVHD occurs. The host's CD4+ cells are stimulated by cytokines released from the damaged tissue.
• Activated CD4+ cells cause the graft to activate T killer and NK cells, which initiate an immune response against the host's susceptible tissues (epithelial tissue, GI tract, and hepatocytes) in phase 2 of GVHD.
Phase 3 of GVHD sees the onset of host tissue injury from immune cells and cytokines.


Evaluation and Diagnostic Results
• The peripheral blood test reveals Howell-Jolly bodies, anemia, thrombocytopenia, and an increase in eosinophils.
• raised LE and liver biopsy; raised serum levels of IL-2 receptor alpha, TNF receptor 1, IL-8, and hepatocyte growth factor.
• tests such as the US, CT scan, and Doppler to evaluate the liver.
• A gastrointestinal system endoscopy.

Complications include liver failure, infection, bleeding, and graft failure, all of which can be fatal.
• The GI system and skin epithelium becoming permanently scarred.

Medical Attention and Surgical Procedure
• the elimination of donor T cells.
• Anti-TNF medications, DMARDs, and immunosuppressive drugs.
• Host CD4+ cell plasmapheresis.
• Inform the customer that steroids and immunosuppressive medications may be administered before a bone marrow or stem cell transplant.
• Keep an eye on your liver enzymes, blood chemistries, and periodic CBC.  This illness appears three and a half months after transplant.

What is Pathology - Multiple Myeloma
Pathophysiology
• Mutation of plasma cells, a type of B-lymphocyte, which invade the GI system, bone marrow, liver, spleen, lymph nodes, lungs, and adrenal glands.
• The outlook for MM is poor.

Evaluation and Diagnostic Results
• Joint pain, low-grade fever, and general malaise. Bone discomfort, particularly in the back or ribs.
• Pneumonia, spinal nerve compression, pathologic fractures, and hypercalcemia.
• The CBC reveals anemia, fluctuating WBC counts, and low platelet counts.
• Bone scans, MRIs, CT scans, and X-rays all reveal serious osteoporosis.
• M-type gamma globulins, also known as Bence-Jones protein, are detected in the urine. (24-hour urine).
• A biopsy of the bone marrow reveals the existence of immature plasma cells.


Complications
• Renal calculi from hypercalcemia, pathologic fractures, spinal cord compression with lack of bowel and bladder control, and GVHD.
• Sepsis, pneumonia, and recurrent illnesses.

Medical Attention and Surgical Procedure
• Thalidomide, IV biphosphonates, high-dose steroids, and analgesics.
• Care for kidney calculi, dehydration, respiratory infections, hypercalcemia, and hyperuricemia.
• External beam radiation treatment combined with high-dose chemotherapy.
• Teach the client to stay hydrated, walk as allowed, and stay safe.
• Immediately report any fever, discomfort, or paresthesias.
• Keep a close eye on your CBC, vital indicators, oxygen saturation, and breath sounds.
• As allowed ovulation.
• Carefully raise the client using a lift sheet, allowing for passive and active range of motion.
• Promote up to 4 litres of fluid consumption per day; treat pain as necessary with medication.

What is Pathology – Leukemia
Pathophysiology Lymphocytes, monocytes, granulocytes, erythrocytes, and platelets can all be impacted by acute or persistent leukaemia. Immature WBCs (blasts) multiply uncontrollably in the bone marrow, lymph tissue, and spleen as a result of a mutation in the bone marrow stem cells. In the bone marrow, the normal WBCs, RBCs, and platelets are significantly outnumbered by the immature and useless WBCs.
• Some types are ALL, AML, CLL, and CML.

Evaluation and Diagnostic Results
• A low platelet count, low RBC count, and a high proportion of underdeveloped WBCs in the CBC.
• Bone marrow extraction, with a cell count revealing a high proportion of immature blasts.
• Examinations for the Philadelphia chromosome in genetics
(CML).
• LP to detect blasts in CSF and establish whether the central nervous system was affected.
• Low-grade fever, paleness, sluggishness, confusion, SOB, bone soreness, headache, and SOB.
• Thrombocytopenia, petechiae and bleeding, infection, GVHD, and serious anaemia are among the
complications.

​Chemotherapy, radiation treatment, stem cell transplants, and bone marrow transplants are among the medical and surgical procedures available.
• Inform customers that the cure rate for ALL in children is high. (cancer-free for 5 years or more).
• Leukemia patients should avoid organic vegetables, use soft toothbrushes, consume moderately warm foods, take frequent breaks from activity, and report fevers right away.
• Regularly check the CBC, vital indicators, and oxygen saturation levels.
• Continue reverse seclusion for the BMT patient.

What is Pathology – Hypertension
Pathophysiology • CO, which is calculated by multiplying the pulse rate by the stroke volume, determines blood pressure (BP). The stimulation of the SNS in response to arterial baroreceptors that measure blood pressure and chemoreceptors that measure carbon dioxide levels can both influence heart rate. The renin-angiotensin-aldosterone system, exercise, emotions, and taking medications that induce vasoconstriction are additional mechanisms that affect blood pressure. PVR is the resistance to blood flow through arterioles that results in a high afterload. High blood pressure damages the intima of arteries, allowing for the infiltration of macrophages, muscle fibers, cholesterol, and fatty acids that create atherosclerotic plaque.

Evaluation and Diagnostic Results
• The optimal systolic and diastolic blood pressure values are less than 120 mm Hg and 79 mm Hg, respectively.
(JNC 7).
• If the average blood pressure readings obtained on two different instances are greater than 139 mm Hg systolic and greater than 89 mm Hg diastolic, hypertension is deemed to exist.

Complications
• Vascular disease and atherosclerosis; chronic heart failure brought on by myocardial infarction (MI) and cerebrovascular accident (CVA); (CHF).
• Retinal and kidney disease brought on by inadequate circulation.

Medical Attention and Surgical Procedure
• Diuretics, blood pressure medications, and dietary adjustments.
• A programme to stop smoking.
• Instruct clients to alter modifiable risk factors, stay away from added salt, consume less caffeine and alcohol, take their recommended medications on schedule, and reduce tension through exercise or meditation.
• Carefully check the patient's blood pressure the right way, with the client sitting and the sphygmomanometer at heart level. After five minutes of relaxation, take your blood pressure.

What is Pathology - Aortic Aneurysm
Pathophysiology

• Aortic ballooning or bulging brought on by genetic abnormalities, smoking, chronic obstructive pulmonary disease, hypertension, atherosclerosis, or hypertension. prevalent in the abdominal artery (abdominal aortic aneurysm [AAA]). Fusiform, saccular, and dissecting types are among those that can occur in families with Marfan's syndrome. until it ruptures, may be entirely asymptomatic.

Evaluation and Diagnostic Results

• Relief from nausea, bloating, or abdominal discomfort after changing positions. abdomen-wide bulk that pulses.
• Auscultation with the stethoscope's ring to listen for bruits close to the umbilicus.
• US screening for males who are 50 years of age or greater or have a family history.
• An enlarged black tumour is visible on an MRI, and the aortic abnormality is visible on an aortogram.
• A spiral CT image with contrast that shows the aneurysm's calcified rim.

Aneurysm rupture, cardiac arrest, hemorrhage, shock, and mortality are all complications.

Medical Attention and Surgical Procedure
• Measurement of the aneurysm's girth.
Antihypertensive drugs for controlling blood pressure.
• A programme to stop smoking.
• Surgical intervention using endovascular grafting or open surgery for healing.
• Educate clients who have a first-degree cousin who has AAA about the risk factors and symptoms to report, and promote ultrasound screening.
• Instruct clients who are at risk to continue their antihypertensive medication treatment, give up smoking, and get yearly physicals.
• As people age or have surgery, the incidence of rupture rises.
• Measure blood pressure and counsel patients having surgery to refrain from lifting heavy objects.

What is Pathology - Raynaud’s Disease
Pathophysiology
• A condition that only affects women, RD produces ischemia and vasospasm at the tips of the nose, fingers, hands, feet, and toes in response to exposure to cold temps or objects. Hyperemia is experienced after ischemia. When ischemic attacks continue for two or more years, a diagnosis is established.
Secondary RD is linked to autoimmune/collagen diseases, people with jobs that require vibratory tools like jackhammers, and endothelin-1 and angiotensin may be the cause.
​
Evaluation and Diagnostic Results
• Thyroid panel to check for metabolic disorders; CBC to check for blood disorders; BUN and creatinine to check for renal and hydration state; PT and aPTT to check the clotting cascade; serum glucose; and PT and aPTT to check the clotting cascade. Additionally, tests are requested for autoimmune and collagen diseases.
• A vasodilator known as calcitonin gene-related peptide is discovered to be reduced in RD.
The vasoconstrictor neuropeptide Y is abundant in secondary RD.

Complications include tissue loss, necrosis, and digital ulceration.

Medical Attention and Surgical Procedure
• SSRIs, analgesics, vasodilators, ACE inhibitors, angiotensin-receptor blockers, analgesics, and lidocaine local infiltration.
"Digital sympathectomy."
• Omega-3 fatty acids of pharmaceutical quality.
• Biofeedback; avoiding cold touch; and quitting smoking.
• Instruct the customer to never smoke and to protect their hands, feet, and face from cold temperatures.
• Immediately report any ischemic episodes.
• Evaluate the nose's hue, sensation, and temperature; smoking cessation programme.

What is Pathology - Buerger’s Disease
Pathophysiology
• BD, also referred to as thromboangiitis obliterans, is a condition characterised by recurrent inflammation of the small and medium arteries in the legs, which leads to the development of thrombi. Young males who smoke (ages 25 to 40) are affected.
It is believed that certain ingredients in tobacco products cause these young males to experience an autoimmune reaction. Vasospasm and a reduction in capillary blood flow take place.

Evaluation and Diagnostic Results

• The five Ps: pallor, paralysis, paresthesia, and pulselessness.
• Leg heaviness and pain that subsides with rest after a brief time of exertion.
In both the upper and lower limbs, ABI measures BP.
Ankle blood pressure drops after a brief time of exercise in the client with PAD, indicating constriction and reduced perfusion.
Doppler ultrasound equipment detects blood flow velocity.
• Images from MRIs depict artery blockage.
• Angiography and plethysmography to see the flow of blood through the limb.

Necrosis, vascular ulcerations, gangrene, and amputation are all complications.


Medical Attention and Surgical Procedure
Vasodilators, calcium channel blockers, anticoagulants, pentoxifylline (to improve red blood cell movement), and others.
• Amputee.
• A programme to stop smoking.
• Emphasize to the customer the value of quitting smoking.
• Direct the individual to a Buerger's disease support group.
• When dependent, the legs will be purple-red and paler when raised; check the pulses.
• Continue your vasodilator and anticoagulant treatment.
• Evaluate the efficacy of support group interactions and smoking cessation programmes.