1.

PATHOPHYSIOLOGY OF DIABETES MELLITUS

Modifiable Risk Factors:
Non-Modifiable Risk
Eating too much Factors:
sweets
Family History
Diet and Exercise of DM

Sedentary lifestyle Age above 40

Stress and Coping Obesity

INSUFFICIE
Frequent or NT Gender
chronic infections INSULIN
Knowledge/Int
elligence

Reduced
tissue uptake
of glucose

Intracellul Extracellul
ar ar
Hypoglyce Hypoglyce
mia mia
Blood glucose
Glucogenesi Hyperosmotic <
s and plasma renal
threshold
gluconeogen
esis
Glycosuria-
Dehydratio
urine has
Breakdow n of cells
high SG
n of fats

Hyperglyce Osmotic
Diuresis -
Decreased of mic coma polyuria
protein synthesis -polydipsia
Cachexia -hypokalemia
Lethargy -hyponatremia
Polyphagia
Decreased
High gamma globulins
levels of Susceptibility to
infections
ketones Impaired wound
healing

Diabetic
ketoacido
sis
 “Pheochromocytoma Treatment (PDQ®): Treatment - Health Professional Information
2. PHEOCHROMOCYTOMA
[NCI]”

Pheochromocytoma is a rare tumor of chromaffin cells most commonly arising from the
adrenal medulla. An estimated 800 cases are diagnosed yearly in the United States. The peak
incidence is in the third to fifth decades of life. Bilateral disease is present in approximately
10% of patients. Bilaterality is much more common in familial pheochromocytoma and is
often found in association with the familial multiple endocrine neoplasia syndromes (MEN,
types 2A and 2B). In patients with MEN type 2 syndromes, the risk of developing a
contralateral tumor following unilateral adrenalectomy is approximately 50%.Other
syndromes associated with pheochromocytoma include neurofibromatosis, von Hippel-Lindau
disease, cerebellar hemangioblastoma, Sturge-Weber syndrome, and tuberous sclerosis. In a
series of 82 unselected patients with pheochromocytoma, 23% were found to be carriers of
associated familial disorders.Therefore, all patients with pheochromocytomas should be
screened for MEN2 and von Hippel-Lindau disease to avert further morbidity and mortality in
the patients and their families. Extra-adrenal pheochromocytoma or functional paraganglioma
occurs in approximately 10% to 15% of cases and may arise from any extra-adrenal
chromaffin tissue in the body associated with sympathetic ganglia.

Extra-adrenal pheochromocytoma is most often located within the abdomen and may have
greater malignant potential than adrenal pheochromocytoma. Extra-adrenal tumors usually
have a poorer prognosis than adrenal tumors. In one series of 73 patients referred to tertiary
care centers, however, no difference was found in the metastatic potential or the prognosis of
extra-adrenal tumors compared to adrenal tumors.Because of the production and release of
catecholamines, pheochromocytomas cause hypertension. Only 0.1% to 0.5% of all
hypertension patients, however, will be found to have a pheochromocytoma. The importance
of the recognition of this disease is that more than 90% of patients properly diagnosed and
treated are curable.

The hypertension caused by pheochromocytoma may be sustained or paroxysmal and is often

severe with occasional malignant features of encephalopathy, retinopathy, and proteinuria.
Less commonly, severe hypertensive reactions may occur during incidental surgery, following
trauma, exercise, or micturition (in the setting of bladder pheochromocytoma) when the
diagnosis is unsuspected. Other clinical features of pheochromocytoma include headache,
sweating, palpitation, tachycardia, and severe anxiety along with epigastric or chest pain.
Orthostatic hypotension is frequently present and is probably caused by reduced intravascular
volume following chronic adrenergic stimulation.

The diagnosis of pheochromocytoma is established by the demonstration of elevated 24-hour

urinary excretion of free catecholamines (norepinephrine and epinephrine) or catecholamine
metabolites (vanillylmandelic acid and total metanephrines). The measurement of plasma
catecholamines can also be of value in the diagnosis of pheochromocytoma. The
measurement of plasma catecholamines, however, has limited sensitivity and specificity.
Plasma metanephrines have been reported to be more sensitive than plasma catecholamines.
When 52 patients with pheochromocytoma were studied, every patient was found to have
elevated plasma levels of metanephrines, but eight of the patients had normal levels of
plasma catecholamines. Pharmacologic testing with agents such as glucagon or clonidine is
rarely required to make the diagnosis

Surgical resection is the standard curative modality.[17] If the primary tumor is localized to
the adrenal gland and is benign, then survival is that of the normal age-matched population.
In patients with unresectable, recurrent, or metastatic disease, long-term survival is possible;
the overall 5-year survival, however, is less than 50%. Pharmacologic treatment of the
catecholamine excess is mandatory and surgery, radiation therapy, or chemotherapy may
provide palliative benefit.
MY REACTION:

There is this so called treatment for this but in some instances,

although it’s very seldom, people who got this disease was at risk of many

kinds of complications. This just serves as a resource to inform and assist clinicians

who care for patient with this disorder. The certain article educates the reader’s regarding the

certain disease and simply it indicates particular information that mainly promotes it

awareness to the readers. Data suggest that for patients with resectable, benign

pheochromocytoma, the overall survival is equal to that of the age-matched normal

population.
3. Differentiate Cushings versus Addison. Use a tabular presentation.

CUSHING’S DISEASE

• disorder caused by high levels of cortisol (hypercortisolism) in the blood.

• S/S: weight gain,

 • hyperhidrosis (excess sweating),

• red striae (the weight gain in Cushing's syndrome stretches the skin, which is thin and

weakened, causing it to hemorrhage) ,

• proximal muscle weakness (hips, shoulders),

• hirsutism(facial male-pattern hair growth),

• baldness and/or cause hair to become extremely dry and brittle. In rare cases, Cushing's

can cause hypercalcemia, which can lead to skin necrosis.

• reduced libido,

• impotence,

• amenorrhoea/oligomenorrhea andinfertility due to elevations in androgens.

• Patients frequently suffer various psychological disturbances, ranging

from euphoria to psychosis.

Mnemonic
C - Central obesity, Cervical fat pads, Collagen fibre weakness, Comedones
(acne)
U - Urinary free cortisol and glucose increase
S - Striae, Suppressed immunity
H - Hypercortisolism, Hypertension, Hyperglycaemia, Hirsutism
I - Iatrogenic (Increased administration of corticosteroids)
N - Noniatrogenic (Neoplasms)
G - Glucose intolerance, Growth retardation
ADDISON’S DISEASE

• It is a rare endocrine disorder wherein the adrenal glands produce insufficient steroid

hormones (glucocorticoids and often mineralocorticoids).

• S/S: The most common symptoms are fatigue,

• lightheadedness upon standing or while upright,

• muscle weakness,

• fever,

• weight loss,

• difficulty in standing up, anxiety,

• nausea,

• vomiting,

• diarrhea,

• headache,

• sweating,

• changes in mood and personality,

• joint and muscle pains.

• Some have marked cravings for salt or salty foods due to the urinary losses of sodium
 • Affected individuals may note increased tanning since adrenal insufficiency is manifested in

the skin primarily by hyperpigmentation.

4. Make a nursing care plan for a hypothetical client with Diabetes Insipidus.
Assessment Nursing Planning Nursing Rationale Evaluation
diagnosis Intervention
• blood Fluid volume Patients will Weigh patient Changes in weight Patient able to
electrol deficit maintain daily. can provide maintain weight.
ytes ca urine output information on fluid
n >30 ml/hr, BP balance and the
reveal > 90/60, HR adequacy of volume
a 60-100 and Measure and record replacement. 1lb =
high so glucose 70- urine output hourly; 2.2kg. Intake equal to
dium le 200 mg/dl. report urine output Fluid volume deficit output.
vel Patient will less than 30ml for 2 reduces glomerular
(hyper demonstrate consecutive hours. filtration and renal
natrem elastic skin blood flow causing
ia as d turgor and oliguria. The
ehydra moist, pink Assess skin turgor, patient in DKA may Membranes pink
tion de mucous mucous membranes also be undergoing and moist, no
velops) membranes. and complaints of osmotic diuresis tenting.
. thirst. and have excessive
• low outputs.
specifi Measure vital signs,
c urine including CVP Poor turgor, dry V/S goes
gravity (central venous membranes and normal.
pressure). excessive thirst are
• -poor
skin all signs of
turgor dehydration.
• -Dry
skin
Compensatory
mechanisms result
in peripheral
vasoconstriction
with a weak thready
pulse, drop in
systolic blood
pressure, orthostatic
hypotension and
reduced CVP.