DISEASE

PATHOPHYSIOLOGY

SIGNS AND SYMPTOMS

- Tiredness and weakness - Fluid which leaks from the bloodstream and builds up in the legs (edema) and abdomen (ascites) - Loss of appetite, feeling sick, and vomiting. - Weight loss (although you may put on weight if you retain a lot of fluid). - A tendency to bleed and bruise more easily. - Jaundice due to a build up of bilirubin. - Itch - due to a build up of toxins. - Mental health changes develop in severe cases as toxins build up in the bloodstream and affect the brain. This can cause changes to your personality and behaviour, confusion, forgetfulness, difficulty concentrating. Eventually it can lead to loss of consciousness, and 'hepatic coma - Spider angiomata or spider nevi. - Palmar erythema - Hypertrophic osteoarthropathy. Chronic proliferative periostitis of the long bones that can cause considerable pain. - Dupuytren's contracture. Flexion deformities of the fingers. - Gynecomastia. - Hypogonadism. Manifested as impotence, infertility, loss of sexual drive, and testicular atrophy - Liver size. Can be enlarged, normal, or shrunken. - Splenomegaly (increase in size of the spleen). - Caput medusa - Fetor hepaticus. Musty odor in breath as a result of increased dimethyl sulfide. - Asterixis Bilateral asynchronous flapping of outstretched, dorsiflexed hands

DIAGNOSTIC TESTS
*The gold standard for diagnosis of cirrhosis is a liver biopsy (architectural distortion of the liver parenchyma with formation of regenerative nodules) - Liver function test: deranged - AST and ALT: - Alkaline phosphate: - Bilirubin: - Albumin: - Prothrombin time: - Globulins: - Serum Na: - Platelet count: - Antibodies to hepatitis C: present - hepatitis B antigen: present - Total iron: - ANA: present in autoimmune hepatitis - Abdominal ultrasound: liver surface nodularity, small liver, possible hypertrophy of left/caudate lobe, ascites, splenomegaly, increased diameter of the portal vein (13 mm), or collateral vessels - Abdominal CT or MRI: liver surface nodularity, small liver, possible hypertrophy of left/caudate lobe, evidence of ascites, or collateral circulation - Upper GI endoscopy: gastrooesophageal varices, portal hypertensive gastropathy - Paracentesis: to examine ascetic fluid for cell, protein and bacterial counts.

NURSING DIAGNOSIS
-Excess Fluid Volume related to electrolyte imbalance and hypoalbuminemia as manifested by ascites and peripheral edema. - Imbalanced Nutrition: Less than body requirements related to anorexia - Disturbed Thought Processes related to effects of high ammonia level. - Disturbed Body Image - Activity Intolerance - Risk for Injury - Risk for Hemorrhage

CIRRHOSIS
- Cirrhosis is a potentially life-threatening condition that occurs when scarring damages the liver. This scarring replaces healthy tissue and prevents the liver from working normally. Cirrhosis usually develops after years of liver inflammation. When chronic diseases cause the liver to become permanently injured and scarred, the condition is called Cirrhosis. - It is a consequence of chronic liver disease characterized by replacement of liver tissue by fibrous scar tissue as well as regenerative nodules (lumps that occur as a result of a process in which damaged tissue is regenerated) leading to progressive loss of liver function. -Cirrhosis is most commonly caused by alcoholism, hepatitis B and C, and fatty liver disease. - It is a condition responsible for 1.2% of all U.S. deathsthe 9th leading cause of death. Three major forms: Leannecs(alcohol induced) Cirrhosis Postnecrotic (micronodular) Cirrhosis Biliary Cirrhosis

PREDISPOSING FACTOR GENDER: MALE AGE: 45-75 RACE: ASIAN & AFRICAN BILIARY ATRESIA

PRECIPITATING FACTOR CHRONIC ALCOHOLISM CHRONIC VIRAL HEPATITIS (TYPE B, C & D) SMOKING MALNUTRITION

DAMAGE TO HEPATIC CELLS

NECROSIS OF HEPATOCYTES

Formation of scar tissue

liver function Obstruction in the hepatic portal circulation Blood back flows into the GI tract

Decreased metabolism of the protein by liver

Decreased colloid osmotic pressure Fluids accumulate in the peritoneal cavity

Accumulation of fluids in the interstitial space

Distended blood vessels

metabolisms of ammonia

Impaired GI function with impaired liver Function

drug metabolism production of clotting factors stores of vitamins and minerals glycogenolysis

PANCREATITIS
- Inflammation of the pancreas, ranging from mild edema to extensive hemorrhage, resulting from various insults to the pancreas. - Defined by a discrete episode of abdominal pain and serum enzymes elevations -Function and structure usually return to normal after an acute attack Two main categories: Acute pancreatitis is characterized by painful episodic inflammation that may, in some patients, lead to damage or destruction of pancreatic tissue, a condition called chronic pancreatitis. Approximately 2000 patients per year die from complications related to AP Chronic pancreatitis (CP) is an inflammatory condition affecting the pancreas and involves progressive, irreversible damage to the pancreatic tissue. Early chronic pancreatitis may begin with recurrent bouts of acute pancreatitis until later development (over several years) of permanent structural and/or functional impairment. In developed countries, this disorder is related to alcohol abuse in approximately 60% to 70% of cases.
Damage to pancreatic cells
Hypertriglyceridemia = Heredity Pancreatic malignancy Post-endoscopic retrograde cholangiopancreatography (ERCP) (2% to 3%) Trauma Infections (mumps, mycoplasma, Epstein-Barr virus, Ascaris lumbricoides, HIV-related co-infections) Drugs (sulphonamides, azathioprine, thiazides, furosemide, oestrogens, valproic acid) [11] Autoimmune conditions (collagen vascular diseases) Pancreas divisum Sphincter of Oddi dysfunction

- abdominal pain, usually constant, midepigastric or periumbilical, radiating to the back or flank - nausea and vomiting - fever - involuntary abdominal guarding, epigastric tenderness - dry mucous membranes, hypotension, cold clammy skin, cyanosis or tenderness, tachycardia and mild to moderate dehydration - shock with respiratory distress and acute renal failure - purplish discoloration of the flanks (Turners sign) or of the periumbilical area (Cullens sign)

*gold standard for Diagnosing CT-SCAN Amylase (80-180 u/L) Lipase Glucose Alkaline Phosphatase Lactate dehydrogenase Cholesterol * Serum albumin, calcium, sodium, magnesium and potassium may be low due to dehydration * Abdominal x-ray to detect an ileus or isolated loop of small bowel overlying pancreas * Chest x-ray for detection of pulmonary complications

Inflammation

Edema of the pancreas & pancreatic duct

-Pain (acute or chronic) related to inflammation, edema, and peritoneal irritation. -Ineffective breathing pattern related to severe pain and pulmonary infiltrates. - Imbalanced Nutrition: less than body requirements related to reduced food intake and increase metabolic demands. - Impaired skin integrity related to poor nutritional status.

Obstruction to the flow of pancreatic enzymes

Activation of pancreatic enzymes inside pancreas

Autodigestion of pancreas

Fatty necrosis, ulceration, hemorrhage, infection

DIABETES MELLITUS II -Formerly non-insulin dependent diabetes mellitus (NIDDM) or adult-onset diabetes -It is a metabolic disorder that is characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency. Diabetes is often initially managed by increasing exercise and dietary modification. If the condition progresses, medications may be needed. Often affecting the obese, diabetes requires patients to routinely check their blood sugar. Type 2 diabetes mellitus is a progressive disorder defined by deficits in insulin secretion and action that lead to abnormal glucose metabolism and related metabolic derangements. Although the aetiologies of type 1 and type 2 diabetes differ dramatically, both lead to hyperglycaemic states, and both share common macrovascular (coronary heart, cerebrovascular, and peripheral vascular disease) and microvascular (retinopathy, nephropathy, and neuropathy) complications. Type 2 diabetes is usually diagnosed based on screening. Filipinos are at higher risk for type 2 diabetes than the U.S. nonHispanic white population.

1st tests to order

Obesity Age: > 30 Diet: fat, sweets Sedentary lifestyle Heredity Stress Gestational Diabetes Mellitus

-fatigue (common) * Increased fatigability may be an early warning sign of progressive cardiovascular disease; clinicians should have a low threshold for cardiac evaluation. -blurred vision (common)

HbA1c: 6.5% or greater fasting plasma glucose: >6.9 mmol/L (>125 mg/dL) random plasma glucose: 11.1 mmol/L (200 mg/dL) 2-hour post-load glucose after 75 g oral glucose: 11.1 mmol/L (200 mg/dL) Tests to consider fasting lipid profile: may show high LDL, low HDL, and/or high triglycerides urine microalbumin: may show microalbuminuria serum creatinine and estimated GFR: may show renal insufficiency ECG: may indicate prior ischaemia dilated retinal examination: may show retinopathy

blood glucose in the blood

Prolonged stimulation of insulin receptors cite of the cells Prolonged stimulation of pancreas to release insulin

* Due to elevated glucose. -paraesthesias (common) * May occur in the extremities as a result of neuropathy in those with prolonged undiagnosed diabetes. -polydipsia (uncommon) * Usually in patients with fasting plasma glucose >16.6 mmol/L (>300 mg/dL), HbA1c >11%. -polyphagia (uncommon) * Usually in patients with fasting plasma glucose >16.6 mmol/L (>300 mg/dL), HbA1c >11%. -polyuria (uncommon) * Usually in patients with fasting plasma glucose >16.6 mmol/L (>300 mg/dL), HbA1c >11%. -nocturia (uncommon)

Exhaustion of beta cells Down regulation of receptor or insulin cellular resistance

-Decreased Cardiac Output -Altered comfort -lmbalanced Nutrition: Less than body requirements -Fluid volume deficit -Disturbed Sensory Perception -Risk for Injury -Activity Intolerance -Risk for Infection

Limited insulin production

Inability of glucose to enter cells

Hyperglycemia (persistent hyperglycemia and continuous insulin resistance)

Osmotic diuresis

Glycosuria and dehydration

* Due to glucose-induced diuresis. -unintentional weight loss (uncommon)

HHNKS (no ketone formation)

* If marked hyperglycaemia is present. -acanthosis nigricans (uncommon)

Intracellular hypoglycemia

Extracellular hyperglycemia

* A velvety, light brown-to-black marking, usually on the neck, under the arms, or in the groin. Can occur at any age. Most often associated with obesity

HYPERTHYROIDISM

-It is a disorder that is caused output by of excessive to stimulation thyroid circulating immunoglublobulins (IgG) factor trigger and that G other might the

Predisposing Factor:

Precipitating Factor: Severe emotional stress Emotional Shock Infection (thyroiditis)

Gender (Female) Age (below 40 years old) Autoimmune disorder (immnunoglobulin G)

thyroid hormone due abnormal of gland the by

Cardiovascular: Increase heart rate Increase o2consumption Hypertension Palpitations Possible heart failure Gastrointestinal: Increase appetite Weight loss Diarrhea Increase gastrointestinal secretions Musculoskeletal: Fatigue Muscle weakness Tremors Integumentary: Diaphoresis Warm skin Hair: soft, straight, possible hair loss Heat intolerance Neurologic: Increase deep tendon reflux Nervousness, restlessness Anxiety Reproductive: Female: Ammenorhea Irregular menses Decrease fertility Male: Impotence Decreased libido Decreased sexual development

Increase thyroid hormone PRODUCTION (T3 AND T4)

HYPERMETABOLISM

PRODUCTION OF THYROID STIMULNG ANTIBODIES (TSIs)

Serum T4 concentration Serum T 3 concentrations Thyroid- binding globulin ( TBG) Triiodothyroxine (T 3) renin uptake TSh radioimmunoassay TSH stimulation Test Thyroid level test RAIU Thyroid Scan Thyroid ultrasound Thyroid antibody test Thyroid- stimulating immunoglobulins (TSI) Basal metabolic rate Serum Cholesterol level

stimulation of TSH to produce T3 and T4.

TSIs react with eye muscle

exopthalmus

Overworked thyroid

SNS stimulation

Hyperactive GI system

- Hyperthermia related to increased metabolic rate - Activity intolerance related to generalized weakness and decreased cardiac reserve. - High risk for visual alteration related to environmental agents. - Imbalanced nutrition less than body requirements related to increased metabolic rate. - Ineffective individual coping related to personal vulnerability to environmental stimuli.

cardiac output

RR

HYPOTHYROIDISM

Early symptoms Predisposing Factors: Genetic Gender: female Age: >40 y.o.
Precipitating Factors: Hashimotos Thyroiditis Antithyroid Drugs Idiopathic External radiation to the Neck Thyroidectomy Pregnancy

It is a condition characterized by abnormally low thyroid hormone production. There are many disorders that result in hypothyroidism. These disorders may directly or indirectly involve the thyroid gland. Because thyroid hormone affects growth, development, and many cellular processes, inadequate thyroid hormone has widespread consequences for the body. Primary thyroid gland is the most common forms include Hashimoto's thyroiditis (an autoimmune disease) and radioiodine therapy for hyperthyroidism.
Secondary pituitary gland occurs if the pituitary gland does not create enough thyroid stimulating hormone (TSH) to induce the thyroid gland to produce enough thyroxine and triiodothyronine. Although not every case of secondary hypothyroidism has a clear-cut cause, it is usually caused by damage to the pituitary gland, as by a tumor, radiation, or surgery.[5] Tertiary hypothalamus results when the hypothalamus fails to produce sufficient thyrotropinreleasing hormone (TRH). TRH prompts the pituitary gland to produce thyroid stimulating hormone (TSH). Hence may also be termed hypothalamic-pituitaryaxis hypothyroidism.

Decreased production of thyroid hormones

Decreased metabolic rate

FSH, LH and prolactin

Poor muscle tone (muscle hypotonia) Fatigue Cold intolerance, increased sensitivity to cold Depression Muscle cramps and joint pain Carpal Tunnel Syndrome Goitre Thin, brittle fingernails Thin, brittle hair Paleness Osteoporosis Decreased sweating Dry, itchy skin Weight gain and water retention Bradycardia (low heart rate less than sixty beats per minute) Constipation Late symptoms

Free triiodothyronine (fT3) Free levothyroxine (fT4) Total T3 Total T4 24 hour urine free T3 Antithyroid antibodies for evidence of autoimmune diseases that may be damaging the thyroid gland Serum cholesterol which may be elevated in hypothyroidism Prolactin as a widely available test of pituitary function Testing for anemia, including ferritin Basal body temperature

anovulation

CNS function

Slow speech and a hoarse, breaking voice deepening of the voice can also be noticed Dry puffy skin, especially on the face Thinning of the outer third of the eyebrows (sign of Hertoghe) Abnormal menstrual cycles Low basal body temperature Less common symptoms Impaired memory Impaired cognitive function (brain fog) and inattentiveness A slow heart rate with ECG changes including low voltage signals. Diminished cardiac output and decreased contractility. Reactive (or post-prandial) hypoglycemia Sluggish reflexes Hair loss Gynecomastia

-Chronic low self-esteem - Constipation - Decreased cardiac output - Disturbed body image - Imbalanced nutrition: Less than body requirements. - Excess fluid volume - Ineffective coping - Ineffective tissue perfusion: cardiopulmonary - Risk for impaired skin integrity

Thyroid tries to produce thyroid hormones

GI activity

HR